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<meta name="robots" content="INDEX,FOLLOW,NOARCHIVE" /><meta name="citation_inbook_title" content="Webvision: The Organization of the Retina and Visual System [Internet]" /><meta name="citation_title" content="Fetal Tissue Allografts in the Central Visual System of Rodents" /><meta name="citation_publisher" content="University of Utah Health Sciences Center" /><meta name="citation_date" content="2007/06/25" /><meta name="citation_author" content="Frederic Gaillard" /><meta name="citation_author" content="Yves Sauve" /><meta name="citation_pmid" content="21413373" /><meta name="citation_fulltext_html_url" content="https://www.ncbi.nlm.nih.gov/books/NBK11505/" /><link rel="schema.DC" href="http://purl.org/DC/elements/1.0/" /><meta name="DC.Title" content="Fetal Tissue Allografts in the Central Visual System of Rodents" /><meta name="DC.Type" content="Text" /><meta name="DC.Publisher" content="University of Utah Health Sciences Center" /><meta name="DC.Contributor" content="Frederic Gaillard" /><meta name="DC.Contributor" content="Yves Sauve" /><meta name="DC.Date" content="2007/06/25" /><meta name="DC.Identifier" content="https://www.ncbi.nlm.nih.gov/books/NBK11505/" /><meta name="description" content="Injury to the brain areas concerned with vision can cause a variety of disorders ranging from visual field defects to much more complex deficits, such as visual agnosia. It all depends on the location and the extent of the damage. Injury to the occipital striate cortex results in corresponding homonymous visual field defects where typically all visual capacities are lost in the fields. Injury to occipito-temporal structures can affect discrimination, selection, and recognition of visual stimulus dimensions and, at higher stages of processing, of objects, faces, scenes, and letters (for review, see Zihl (1)) (Fig. 1)." /><meta name="og:title" content="Fetal Tissue Allografts in the Central Visual System of Rodents" /><meta name="og:type" content="book" /><meta name="og:description" content="Injury to the brain areas concerned with vision can cause a variety of disorders ranging from visual field defects to much more complex deficits, such as visual agnosia. It all depends on the location and the extent of the damage. Injury to the occipital striate cortex results in corresponding homonymous visual field defects where typically all visual capacities are lost in the fields. Injury to occipito-temporal structures can affect discrimination, selection, and recognition of visual stimulus dimensions and, at higher stages of processing, of objects, faces, scenes, and letters (for review, see Zihl (1)) (Fig. 1)." /><meta name="og:url" content="https://www.ncbi.nlm.nih.gov/books/NBK11505/" /><meta name="og:site_name" content="NCBI Bookshelf" /><meta name="og:image" content="https://www.ncbi.nlm.nih.gov/corehtml/pmc/pmcgifs/bookshelf/thumbs/th-webvision-lrg.png" /><meta name="twitter:card" content="summary" /><meta name="twitter:site" content="@ncbibooks" /><meta name="bk-non-canon-loc" content="/books/n/webvision/ch34regeneration2/" /><link rel="canonical" href="https://www.ncbi.nlm.nih.gov/books/NBK11505/" /><link rel="stylesheet" href="/corehtml/pmc/css/figpopup.css" type="text/css" media="screen" /><link rel="stylesheet" href="/corehtml/pmc/css/bookshelf/2.26/css/books.min.css" type="text/css" /><link rel="stylesheet" href="/corehtml/pmc/css/bookshelf/2.26/css/books_print.min.css" type="text/css" media="print" /><style type="text/css">p a.figpopup{display:inline !important} .bk_tt {font-family: monospace} .first-line-outdent .bk_ref {display: inline} .body-content h2, .body-content .h2 {border-bottom: 1px solid #97B0C8} .body-content h2.inline {border-bottom: none} a.page-toc-label , .jig-ncbismoothscroll a {text-decoration:none;border:0 !important} .temp-labeled-list .graphic {display:inline-block !important} .temp-labeled-list img{width:100%}</style><script type="text/javascript" src="/corehtml/pmc/js/jquery.hoverIntent.min.js"> </script><script type="text/javascript" src="/corehtml/pmc/js/common.min.js?_=3.18"> </script><script type="text/javascript" src="/corehtml/pmc/js/large-obj-scrollbars.min.js"> </script><script type="text/javascript">window.name="mainwindow";</script><script type="text/javascript" src="/corehtml/pmc/js/bookshelf/2.26/book-toc.min.js"> </script><script type="text/javascript" src="/corehtml/pmc/js/bookshelf/2.26/books.min.js"> </script><meta name="book-collection" content="NONE" />
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<div class="pre-content"><div><div class="bk_prnt"><p class="small">NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.</p><p>Kolb H, Fernandez E, Jones B, et al., editors. Webvision: The Organization of the Retina and Visual System [Internet]. Salt Lake City (UT): University of Utah Health Sciences Center; 1995-. </p></div><div class="iconblock clearfix whole_rhythm no_top_margin bk_noprnt"><a class="img_link icnblk_img" title="Table of Contents Page" href="/books/n/webvision/"><img class="source-thumb" src="/corehtml/pmc/pmcgifs/bookshelf/thumbs/th-webvision-lrg.png" alt="Cover of Webvision" height="100px" width="80px" /></a><div class="icnblk_cntnt eight_col"><h2>Webvision: The Organization of the Retina and Visual System [Internet].</h2><a data-jig="ncbitoggler" href="#__NBK11505_dtls__">Show details</a><div style="display:none" class="ui-widget" id="__NBK11505_dtls__"><div>Kolb H, Fernandez E, Jones B, et al., editors.</div><div>Salt Lake City (UT): <a href="http://webvision.med.utah.edu/" ref="pagearea=page-banner&amp;targetsite=external&amp;targetcat=link&amp;targettype=publisher">University of Utah Health Sciences Center</a>; 1995-.</div></div><div class="half_rhythm"><ul class="inline_list"><li style="margin-right:1em"><a class="bk_cntns" href="/books/n/webvision/">Contents</a></li></ul></div><div class="bk_noprnt"><form method="get" action="/books/n/webvision/" id="bk_srch"><div class="bk_search"><label for="bk_term" class="offscreen_noflow">Search term</label><input type="text" title="Search this book" id="bk_term" name="term" value="" data-jig="ncbiclearbutton" /> <input type="submit" class="jig-ncbibutton" value="Search this book" submit="false" style="padding: 0.1em 0.4em;" /></div></form></div></div><div class="icnblk_cntnt two_col"><div class="pagination bk_noprnt"><a class="active page_link prev" href="/books/n/webvision/ch33regeneration1/" title="Previous page in this title">&lt; Prev</a><a class="active page_link next" href="/books/n/webvision/electroretinography/" title="Next page in this title">Next &gt;</a></div></div></div></div></div>
<div class="main-content lit-style" itemscope="itemscope" itemtype="http://schema.org/CreativeWork"><div class="meta-content fm-sec"><h1 id="_NBK11505_"><span class="title" itemprop="name">Fetal Tissue Allografts in the Central Visual System of Rodents</span></h1><p class="contrib-group"><span itemprop="author">Frederic Gaillard</span> and <span itemprop="author">Yves Sauve</span>.</p><p class="small">Created: <span itemprop="datePublished">May 1, 2005</span>; Last Update: <span itemprop="dateModified">June 25, 2007</span>.</p></div><div class="jig-ncbiinpagenav body-content whole_rhythm" data-jigconfig="allHeadingLevels: ['h2'],smoothScroll: false" itemprop="text"><div id="ch34regeneration2.Introduction"><h2 id="_ch34regeneration2_Introduction_">Introduction</h2><p>Injury to the brain areas concerned with vision can cause a variety of disorders ranging
from visual field defects to much more complex deficits, such as visual agnosia. It all
depends on the location and the extent of the damage. Injury to the occipital striate cortex
results in corresponding homonymous visual field defects where typically all visual
capacities are lost in the fields. Injury to occipito-temporal structures can affect
discrimination, selection, and recognition of visual stimulus dimensions and, at higher
stages of processing, of objects, faces, scenes, and letters (for review, see Zihl (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.1">1</a>)) (<a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F1/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F1" rid-ob="figobch34regeneration2F1">Fig. 1</a>).</p><div class="iconblock whole_rhythm clearfix ten_col fig" id="figch34regeneration2F1" co-legend-rid="figlgndch34regeneration2F1"><a href="/books/NBK11505/figure/ch34regeneration2.F1/?report=objectonly" target="object" title="Figure 1" class="img_link icnblk_img figpopup" rid-figpopup="figch34regeneration2F1" rid-ob="figobch34regeneration2F1"><img class="small-thumb" src="/books/NBK11505/bin/regeneration2f1.gif" src-large="/books/NBK11505/bin/regeneration2f1.jpg" alt="Figure 1. Visual deficits in human and related injured brain regions." /></a><div class="icnblk_cntnt" id="figlgndch34regeneration2F1"><h4 id="ch34regeneration2.F1"><a href="/books/NBK11505/figure/ch34regeneration2.F1/?report=objectonly" target="object" rid-ob="figobch34regeneration2F1">Figure 1</a></h4><p class="float-caption no_bottom_margin">Visual deficits in human and related injured brain regions. A, visual
location (lateral occipital gyrus). B, motion blindness (middle temporal gyrus). C,
achromatopsia (occipito-temporal gyrus). D, visual agnosia (posterior and medial
temporo-occipital <a href="/books/NBK11505/figure/ch34regeneration2.F1/?report=objectonly" target="object" rid-ob="figobch34regeneration2F1">(more...)</a></p></div></div><p>Since the 1970s, numerous investigations have focused on trying to restore lost function by
replacement of injured brain structures with homologous, allogeneic, embryonic neural
tissue. Such approaches have even reached the clinical level as a therapy for the treatment
of some neurological disorders such as Parkinson's and Huntington's diseases. With the
exception of these specific cases, though, we are not yet ready to go to the clinic.
Intracerebral grafting presently remains an experimental model used to address fundamental
questions concerning brain development, neuronal plasticity, regeneration, and formation of
topographic connections. The latter is a minimal requirement for functional recovery in
point-to-point sensory systems such as the visual system (see previous chapter).</p><p>Putting fetal brain tissue grafts in the mature central nervous system (CNS) differs from
peripheral nerve (PN) grafting in at least the following two ways. First, although a PN
graft is used to bridge two brain areas, an intracerebral embryonic tissue graft is meant to
restore the function of the damaged area. The fetal grafted tissue must develop its own set
of connections with the right structures in the host brain, and these connections must be
orderly arranged. Second, although all elements in PN grafting are at the same age, the
intracerebral embryonic tissue graft is heterochronic with respect to the host tissue. For a
short period after implantation, grafted tissue behaves as an immature piece of brain.
Theoretically, this immature status should allow circuitry reconstruction. Donor embryonic
cells have a greater potential for axonal outgrowth and regeneration than mature host
neurons (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.2">2</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.3">3</a>). Thus, they may be better at
establishing contacts with host target cells. Furthermore, the fetal graft may produce
trophic factors or signaling cues, which are present in the brain only at early
developmental stages, and should reactivate neurotropic processes in "dormant" host neuron
populations. For instance, embryonic cortical transplants will produce NT-3, which is absent
from the cortex past 2 weeks of age (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.4">4</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.5">5</a>). In vitro
assays (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.6">6</a>) have shown that
NT-3 has dual effects on layer 2-3 and layer 6 cortical neurons. Fifteen days after implant,
cortical grafts will also produce a glial cell line-derived neurotrophic factor (GDNF), a
potent survival factor for claustral neurons that project to the occipital cortex (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.7">7</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.8">8</a>).</p><p>Unfortunately, there is abundant literature suggesting that environmental constraints from
the mature host brain alter the restorative capacities of fetal grafts in various ways.
First, the mature environment affects both the number of surviving neurons within a graft
and the size of the graft itself (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.9">9-12</a>). Second, the mature CNS environment is non-permissive for axonal
regeneration of host neurons (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.13">13-17</a>) (see section 2 from the previous chapter). Third, the mature CNS
environment is poorly permissive for receiving outgrowing axons from embryonic allogeneic
neurons (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.18">18-23</a>).</p><p>These above-mentioned results suggest that intracerebral embryonic tissue grafts might only
be effective in "diffuse" projection systems, i.e., by exerting a paracrine effect (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.24">24-28</a>). In opposition to this,
a few investigations have demonstrated that such grafts can restore, at least partially,
complex motor behaviors (skilled forelimb reaching for food) that require a precise
interaction between neuronal circuits, much more than expected of paracrine effects (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.19">19</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.29">29</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.30">30</a>). However, even in such reports, the donor
neurons appear to establish a very limited number of connections with the host.</p><p>Pioneer work in the visual system model was done in the mid-1970s by Drs. Raymond Lund and
Alan Harvey and colleagues, who transplanted parts of the embryonic CNS to various brain
locations in neonatal rats (for a review, see Lund (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.31">31</a>)). Most of their studies were focused on CNS
development and, therefore, consisted of examining whether such grafts developed near-normal
architecture and established extensive connections with appropriate host structures. The
outcome of fetal grafts into adult hosts has been studied less extensively, but a limited
number of reports suggest that fetal tissues can integrate functionally within the adult
host CNS. We will review these investigations that, in contrast to the mainstream opinion,
show that tectal and cortical allografts can receive highly ordered inputs and can project
to distant visual targets in the adult brain.</p></div><div id="ch34regeneration2.The_Visual_System_of"><h2 id="_ch34regeneration2_The_Visual_System_of_">The Visual System of Rodents: A Brief Overview</h2><p>Unless reconstruction of neural circuitries comparable to normal in terms of amount,
extension, and topical organization are achieved, we cannot expect complete functional
recovery in point-to-point neural systems. The normal structural and functional organization
of the visual system of adult rodents has been investigated extensively and now forms a
basis for regeneration experiments (for reviews, see Sefton and Dreher (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.32">32</a>), Zilles and Wree (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.33">33</a>), and Sefton et al (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.34">34</a>)). A brief summary of the
major findings is given below for comparative purposes.</p><div id="ch34regeneration2.Retinal_Output"><h3>Retinal Output</h3><p>In the adult rat, virtually all (&#x0003e;95%) retinal ganglion cells (RGCs) project
contralaterally to the superior colliculus (SC) and to the dorsal division of the lateral
geniculate nucleus (DLG). In the SC, axons from the retina enter at the level of the
stratum opticum (SO) and arborize in the SO and the superficial gray layer (SGL). Dense
terminals are also found in lateral posterior nucleus, LP; ventral division of the lateral
geniculate nucleus, magnocellular part, VLG; intergeniculate leaflet, IGL; and pretectal
nuclei (nucleus of the optic tract, OT; olivary pretectal nucleus, OPT; posterior
pretectal nucleus, PPT). Some of these inputs (30-50%) are collateral branches of
retinocollicular axons. A small contingent (&#x0003c;5%) of the RGCs contacts the same
structures ipsilaterally. Thus, each retinorecipient center receives input from both eyes.
Sparse projections are found in the suprachiasmatic nucleus (SCN), the various nuclei of
the accessory optic system, the hypothalamus, and the inferior colliculus. A schematic
view of these connections is given in Fig. 6 of the previous chapter.</p></div><div id="ch34regeneration2.Subcortical_Network"><h3>Subcortical Network</h3><p>The DLG is much more than a relay center for RGC projections to the cortex. In fact, it
receives most of its input from structures other than the retina, namely the visual
thalamic reticular nucleus (Rt), layer 6 small pyramidal neurons in the occipital cortex
(areas 17, 18, 18a; also called, respectively, areas Oc1, Oc2M, Oc2L; or areas V1, V2M,
V2L), the SC (SGL layer), some pretectal nuclei (OT, OPT), and the contralateral
parabigeminal nucleus (PBg), a homolog of the isthmo-optic nucleus in lower vertebrates.
Projections arising from relay cells in the DLG are restricted to Rt (dorsal part) and
occipital cortex.</p><p>The retinorecipient layers of the SC have reciprocal connections with the VLG, the
pretectum, and the ipsilateral PBg nucleus (ventral and dorsal divisions). They receive
further afferents from the contralateral PBg and from layer 5 pyramidal neurons in the
visual cortex. Major efferents go to the DLG, the LP thalamic nucleus, and to the
intermediate (IGL) and deep (DpL) gray layers of the SC, where other sensory systems are
represented. The LP nucleus (equivalent of the LP-pulvinar in cats and of the pulvinar in
primates) has reciprocal connections with visual (mainly Oc2L, layers 5 and 6) and
temporal areas in the ipsilateral cortex. The LP receives additional inputs from the Rt,
zona incerta (ZI), and the pretectum (OT). Neurons in the IGL and DpL layers of the SC
project to various structures in the pons, brain stem, cervical spinal cord, and
hypothalamus.</p><p>The VLG has reciprocal connections with the pretectum (OT, OPT and APT, the anterior
pretectal nucleus), SC (SGL and SO layers), and its contralateral homolog. It receives
further projection from the occipital cortex (layer 5 neurons) and projects to the ZI,
central gray, pons, and the suprachiasmatic nucleus (SCN). Finally, in addition to retinal
and collicular inputs, the pretectum receives cortical afferents from the occipital cortex
and projects to the LP, to the adjacent lateraldorsal (LD) thalamic nucleus (which has
reciprocal connections with the occipital cortex), and to the pons (largely to the
reticulotegmental nucleus) (<a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F2/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F2" rid-ob="figobch34regeneration2F2">Fig. 2</a>).</p><div class="iconblock whole_rhythm clearfix ten_col fig" id="figch34regeneration2F2" co-legend-rid="figlgndch34regeneration2F2"><a href="/books/NBK11505/figure/ch34regeneration2.F2/?report=objectonly" target="object" title="Figure 2" class="img_link icnblk_img figpopup" rid-figpopup="figch34regeneration2F2" rid-ob="figobch34regeneration2F2"><img class="small-thumb" src="/books/NBK11505/bin/regeneration2f2.gif" src-large="/books/NBK11505/bin/regeneration2f2.jpg" alt="Figure 2. Major ipsilateral connections (designed as arrows) of the visual cortex of rodents." /></a><div class="icnblk_cntnt" id="figlgndch34regeneration2F2"><h4 id="ch34regeneration2.F2"><a href="/books/NBK11505/figure/ch34regeneration2.F2/?report=objectonly" target="object" rid-ob="figobch34regeneration2F2">Figure 2</a></h4><p class="float-caption no_bottom_margin">Major ipsilateral connections (designed as arrows) of the visual cortex of
rodents. Green-coded connections are valid for all areas. Specific, additional
connections for Oc1 (area 17) are white coded; those for Oc2M (area 18) are red coded;
and those <a href="/books/NBK11505/figure/ch34regeneration2.F2/?report=objectonly" target="object" rid-ob="figobch34regeneration2F2">(more...)</a></p></div></div></div><div id="ch34regeneration2.Cortical_Network"><h3>Cortical Network</h3><p>Afferents to cortical area Oc1 originate predominantly from the three thalamic relay
nuclei: DLG, LP, and LD. Termination sites are localized in layers 4, lower 3, 6, and 1.
Other thalamic sources are the posterior complex (Po), ventromedian (VM), centromedian
(CM), and the ventrolateral (VL) nuclei. Projections from Po and VM terminate in layer 1;
those from CM and VL in layers 1 and 6. Further afferents are provided by frontal (Fr2),
temporal (Te1-2), retrosplenial (RSA/RSG), perirhinal (PRh), and adjacent visual areas in
the ipsilateral cortex. With respect to this scheme, area Oc2M receives no afferent from
Te2 and PRh but an additional input from orbital cortical areas (MO/VO/VLO), whereas area
Oc2L receives no afferent from Te1 and PRh but an additional input from the hindlimb
region (HL) in the sensorimotor cortex. Afferents from the claustrum (CL) are mostly
distributed in the infragranular layers of Oc1 and/or Oc2M areas (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.35">35</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.36">36</a>). Oc1-2 areas also receive some callosal
inputs from visual areas (layer 2-3 and 5-6 neurons) in the opposite cortex. Callosal
terminations extend throughout the cortical depth at the borders of area Oc1 and adjacent
extrastriate areas as well as in multiple patches through Oc2M-L areas. Prominent labeling
also occurs in the infragranular layers of the temporal cortex. Finally, the visual cortex
and subcortical retinorecipient nuclei both receive nonspecific cholinergic,
noradrenergic, and serotonergic innervations from various structures in the basal
forebrain, from locus coeruleus (LC) and from dorsal raphe nuclei (DR), respectively.</p><p>In addition to reciprocal connections, visual cortical areas have widespread ipsilateral
projections through the normal adult brain. At the cortical level, efferents from area Oc1
are found into the dorsomedial frontal area Fr2 (layers 1 and 6), the ventrolateral
orbital area (VLO), the retrosplenial areas (layers 1 and 6), the perirhinal area (layer
5-6, up to the caudalmost pole of the cortex), and the entorhinal cortex. Additional
efferents originating from area Oc2M are observed in the cingulate area Cg1, the parietal
areas S1-2 (caudal part; layers 1-3 and 6), the temporal areas Te1-3 (layer 1-3 and 6,
mainly), and the claustrum (full extent). Efferents from area Oc2L also target the dorsal
half of the prelimbic cortex (PrL area) as well as lateral, basal, and central amygdaloid
nuclei (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.37">37</a>). Projections
from Oc2 areas to Fr2 and Cg1 extend up to the rostralmost pole of the cortex. At the
subcortical level, Oc1 and Oc2 areas have dense terminals in hippocampal structures
(presubiculum, PrS; and parasubiculum, PaS), striatum (the dorsomedial portion) (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.38">38</a>), visual thalamic nuclei
(DLG, VLG, LP/LD, Po, Rt), ZI, various pretectal nuclei (P-TECT), SGL and IGL layers of
the SC, and pontine nuclei (dorsolateral division) (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.39">39</a>). Contralateral projections are confined to
Oc1-2 and Te1 areas as well as, but sparsely, to the dorsomedial sector of the striatum
and the dorsolateral subdivision of the amygdala.</p></div><div id="ch34regeneration2.Visual_Field_Topogra"><h3>Visual Field Topography</h3><p>Retinofugal axons arising in different retinal quadrants maintain their relative
positions in the optic nerve, lose this initial order as they progress toward the chiasm,
and reform a distinct dorsal-ventral arrangement in the optic tract before reaching
primary visual targets, where they terminate in a precise topographic manner (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.40">40-43</a>). Retinotopy in visual
centers was first seen by Lashley (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.44">44</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.45">45</a>) and then abundantly documented by both
electrophysiological and anatomical approaches (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.46">46-52</a>). Recently, optical imaging techniques
have confirmed all previous findings (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.53">53</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.54">54</a>). A schematic representation of the visual
field topography onto the DLG, SC, and visual cortex is given below (<a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F3/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F3" rid-ob="figobch34regeneration2F3">Fig. 3</a>).</p><div class="iconblock whole_rhythm clearfix ten_col fig" id="figch34regeneration2F3" co-legend-rid="figlgndch34regeneration2F3"><a href="/books/NBK11505/figure/ch34regeneration2.F3/?report=objectonly" target="object" title="Figure 3" class="img_link icnblk_img figpopup" rid-figpopup="figch34regeneration2F3" rid-ob="figobch34regeneration2F3"><img class="small-thumb" src="/books/NBK11505/bin/regeneration2f3.gif" src-large="/books/NBK11505/bin/regeneration2f3.jpg" alt="Figure 3. Schematic representation of the right visual field topography onto the DLG, SC, and visual cortex of normal rats." /></a><div class="icnblk_cntnt" id="figlgndch34regeneration2F3"><h4 id="ch34regeneration2.F3"><a href="/books/NBK11505/figure/ch34regeneration2.F3/?report=objectonly" target="object" rid-ob="figobch34regeneration2F3">Figure 3</a></h4><p class="float-caption no_bottom_margin">Schematic representation of the right visual field topography onto the DLG,
SC, and visual cortex of normal rats. Color code: red, upper nasal field; pink, upper
temporal field; deep blue, lower nasal field; sky blue, lower temporal field.
Subdivisions <a href="/books/NBK11505/figure/ch34regeneration2.F3/?report=objectonly" target="object" rid-ob="figobch34regeneration2F3">(more...)</a></p></div></div><p>At the geniculate level (<a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F3/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F3" rid-ob="figobch34regeneration2F3">Fig. 3</a>, A
and D), the nasal field (temporal retina) is represented caudally and dorsomedially; the
temporal field (nasal retina) occupies most of the rostral part of the nucleus; the lower
field (upper retina) is mostly represented in the caudal part of the nucleus,
lateroventrally; and the upper field (lower retina) projects mainly to the rostral part of
the nucleus, dorsally. The dorsomedial part of the DLG also receives input from the lower
temporal quadrant (red sector; <a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F3/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F3" rid-ob="figobch34regeneration2F3">Fig.
3</a>B) of the ipsilateral retina. On the contralateral SC (<a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F3/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F3" rid-ob="figobch34regeneration2F3">Fig. 3</a>, A and C), the nasal visual field is mapped
rostrally; the temporal visual field, caudally; the upper field, medially; and the lower
field, laterally. In rats, the representation of the central visual field is not
substantially magnified. The ipsilateral retinal contingent projects anteromedially (red
sector; <a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F3/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F3" rid-ob="figobch34regeneration2F3">Fig. 3</a>B).</p><p>At the cortical level (area Oc1/17), the naso-temporal axis of the visual field projects
from lateral to medial, the lower field (upper retina) projects rostrally, and the upper
field projects caudally. A restricted caudal region of area Oc1 receives input from the
ipsilateral retina. The vertical meridian (body axis) is set at the border between area 17
and area 18. Beyond this point, the naso-temporal direction is inverted. Borderline zones
in areas 17 and 18 contain binocular neurons. Multiple ordered representations of the
visual field are present in the adjacent extrastriate areas (for discussion, see Rosa and
Krubitzer (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.55">55</a>)).</p></div></div><div id="ch34regeneration2.Standard_Strategy_fo"><h2 id="_ch34regeneration2_Standard_Strategy_fo_">Standard Strategy for Intracerebral Transplantation: Graft Morphology</h2><p>Grafts usually consist of blocks or sheets of neural tissue excised from 15-16-day-old
(E15-16) embryos, which are put into previously surgically made cavities in the host. Older
grafts survive poorly and have reduced size (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.56">56</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.57">57</a>). Although not critical for axonal sprouting
(see below), delayed implantation has been assumed to enhance cell survival and outgrowth
(<a class="bk_pop" href="#ch34regeneration2.EXTYLES.58">58-60</a>), probably because
endogenous neurotrophic factors can accumulate at the lesion site (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.61">61</a>) (<a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F4/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F4" rid-ob="figobch34regeneration2F4">Fig. 4</a>).</p><div class="iconblock whole_rhythm clearfix ten_col fig" id="figch34regeneration2F4" co-legend-rid="figlgndch34regeneration2F4"><a href="/books/NBK11505/figure/ch34regeneration2.F4/?report=objectonly" target="object" title="Figure 4" class="img_link icnblk_img figpopup" rid-figpopup="figch34regeneration2F4" rid-ob="figobch34regeneration2F4"><img class="small-thumb" src="/books/NBK11505/bin/regeneration2f4.gif" src-large="/books/NBK11505/bin/regeneration2f4.jpg" alt="Figure 4. Basic transplantation protocols." /></a><div class="icnblk_cntnt" id="figlgndch34regeneration2F4"><h4 id="ch34regeneration2.F4"><a href="/books/NBK11505/figure/ch34regeneration2.F4/?report=objectonly" target="object" rid-ob="figobch34regeneration2F4">Figure 4</a></h4><p class="float-caption no_bottom_margin">Basic transplantation protocols. A, for current anatomical studies. Blocks of
embryonic tissue were implanted in aspirated lesion cavities performed in the host brain
3 days earlier. B, used by Girman (71) for
electrophysiological recordings. Grafts are <a href="/books/NBK11505/figure/ch34regeneration2.F4/?report=objectonly" target="object" rid-ob="figobch34regeneration2F4">(more...)</a></p></div></div><p>As in newborns (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.62">62</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.63">63</a>), primary connections with
the host brain appear 3-4 days after transplantation (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.64">64</a>), whereas neovascularization and blood supply
require approximately another week to be completed, a delay that may seriously hamper graft
cell metabolism (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.65">65</a>).
Nonetheless, both graft implantation and development in adults can be as successful as in
neonate recipients (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.62">62</a>,
<a class="bk_pop" href="#ch34regeneration2.EXTYLES.66">66</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.67">67</a>). Investigations are usually performed 3-4
months after grafting.</p><p>In serial histological sections, all implants look like disorganized cellular masses that
are more or less clearly separated from the host tissue by a region of lower cell density or
host white matter. Glial scarring at the host-graft interface, although highly variable, is
usually minimal (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.60">60</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.68">68</a>). At this time point, graft
development is achieved. Most neurons in cortical grafts (60-80%) seem mature (expression of
Hu/Elav proteins) (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.66">66</a>) and
look "normal" at the ultrastructural level (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.69">69</a>). The remaining neurons have immature
characteristics, such as multiple nucleoli or binuclear somas (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.60">60</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.70">70</a>) (<a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F5/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F5" rid-ob="figobch34regeneration2F5">Fig. 5</a>).</p><div class="iconblock whole_rhythm clearfix ten_col fig" id="figch34regeneration2F5" co-legend-rid="figlgndch34regeneration2F5"><a href="/books/NBK11505/figure/ch34regeneration2.F5/?report=objectonly" target="object" title="Figure 5" class="img_link icnblk_img figpopup" rid-figpopup="figch34regeneration2F5" rid-ob="figobch34regeneration2F5"><img class="small-thumb" src="/books/NBK11505/bin/regeneration2f5.gif" src-large="/books/NBK11505/bin/regeneration2f5.jpg" alt="Figure 5. A and B, typical cellular aspect of tectal (from Girman (71)) and occipital (from Domballe et al." /></a><div class="icnblk_cntnt" id="figlgndch34regeneration2F5"><h4 id="ch34regeneration2.F5"><a href="/books/NBK11505/figure/ch34regeneration2.F5/?report=objectonly" target="object" rid-ob="figobch34regeneration2F5">Figure 5</a></h4><p class="float-caption no_bottom_margin">A and B, typical cellular aspect of tectal (from Girman (71)) and occipital
(from Domballe et al. (66)) grafts 3 months
after grafting. Nissl staining. C and D, graft vascularization as observed in wild-type
E15 mouse cortical tissue grafted in an adult <a href="/books/NBK11505/figure/ch34regeneration2.F5/?report=objectonly" target="object" rid-ob="figobch34regeneration2F5">(more...)</a></p></div></div><p>A typical feature of fetal tectal tissue transplants in adult hosts is the presence of
dorsally located, myelinated "fiber-free" areas (<a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F6/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F6" rid-ob="figobch34regeneration2F6">Fig. 6</a>). In addition,
there is a proponderance of cells with small perikarya and short dendrites (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.67">67</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.71">71</a>), a relatively high acetylcholinesterase
(AChE) activity, a high concentration of alpha-bungarotoxin binding sites, and a low number
of neuroglial elements (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.57">57</a>,
<a class="bk_pop" href="#ch34regeneration2.EXTYLES.72">72-74</a>). Similar
characteristics are found in the retinorecipient layers of the SC in normal rats. In neonate
hosts, the "fiber-free" layer over the "fiber-rich" core of the graft (<a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F6/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F6" rid-ob="figobch34regeneration2F6">Fig. 6</a>) is penetrated by regenerated retinal afferents
(<a class="bk_pop" href="#ch34regeneration2.EXTYLES.75">75</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.76">76</a>).</p><div class="iconblock whole_rhythm clearfix ten_col fig" id="figch34regeneration2F6" co-legend-rid="figlgndch34regeneration2F6"><a href="/books/NBK11505/figure/ch34regeneration2.F6/?report=objectonly" target="object" title="Figure 6" class="img_link icnblk_img figpopup" rid-figpopup="figch34regeneration2F6" rid-ob="figobch34regeneration2F6"><img class="small-thumb" src="/books/NBK11505/bin/regeneration2f6.gif" src-large="/books/NBK11505/bin/regeneration2f6.jpg" alt="Figure 6. Typical morphological features of embryonic tectal grafts (sheets of tissue) in neonate hosts." /></a><div class="icnblk_cntnt" id="figlgndch34regeneration2F6"><h4 id="ch34regeneration2.F6"><a href="/books/NBK11505/figure/ch34regeneration2.F6/?report=objectonly" target="object" rid-ob="figobch34regeneration2F6">Figure 6</a></h4><p class="float-caption no_bottom_margin">Typical morphological features of embryonic tectal grafts (sheets of tissue)
in neonate hosts. A, Holmes neurofibrillar staining. Note the fiber-free (ff) area
covering the fiber-rich core of the graft (T). B, Nissl staining. C, widespread retinal
input <a href="/books/NBK11505/figure/ch34regeneration2.F6/?report=objectonly" target="object" rid-ob="figobch34regeneration2F6">(more...)</a></p></div></div><p>Grafts of blocks of fetal cortex lack the typical layered organization when integrating
into the host CNS. Neurons are 60-80% of the normal density and gathered into clusters
separated by myelinated bundles (<a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F7/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F7" rid-ob="figobch34regeneration2F7">Fig. 7</a>, A-C). They also contain high number of
neuroglial and microglial cells (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.69">69</a>). Regardless of their
origin, cortical grafts typically receive diffuse cholinergic and aminergic input, mostly in
their lower part, near the corpus callosum (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.66">66</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.77">77-79</a>).</p><div class="iconblock whole_rhythm clearfix ten_col fig" id="figch34regeneration2F7" co-legend-rid="figlgndch34regeneration2F7"><a href="/books/NBK11505/figure/ch34regeneration2.F7/?report=objectonly" target="object" title="Figure 7" class="img_link icnblk_img figpopup" rid-figpopup="figch34regeneration2F7" rid-ob="figobch34regeneration2F7"><img class="small-thumb" src="/books/NBK11505/bin/regeneration2f7.gif" src-large="/books/NBK11505/bin/regeneration2f7.jpg" alt="Figure 7. Gross morphology of cortical grafts." /></a><div class="icnblk_cntnt" id="figlgndch34regeneration2F7"><h4 id="ch34regeneration2.F7"><a href="/books/NBK11505/figure/ch34regeneration2.F7/?report=objectonly" target="object" rid-ob="figobch34regeneration2F7">Figure 7</a></h4><p class="float-caption no_bottom_margin">Gross morphology of cortical grafts. A, absence of lamination. Cresyl violet
staining. B, typical cell cluster (inset in A). C, intragraft myelin sheets (arrows).
Luxol blue staining. D, distribution of the soma sizes in the normal rat cortex,
responsive <a href="/books/NBK11505/figure/ch34regeneration2.F7/?report=objectonly" target="object" rid-ob="figobch34regeneration2F7">(more...)</a></p></div></div><p>Although roughly similar at a first glance, different cortical grafts show differences in
their neuronal phenotypes. On the basis of Golgi-Cox stained material, Aleksandrova and
Girman (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.80">80</a>) proposed a three-group
classification:</p><ul><li id="A4242" class="half_rhythm"><div>Type I: grafts contain multiple neuron morphologies resembling those in the normal
cortex. The small layer 2-3 pyramids have small or medium perikarya (10-16 and 20-26
&#x003bc;m in diameter, respectively) and apical dendrites running for considerable
distances along the graft boundary with unpredictable orientations.</div></li><li id="A4243" class="half_rhythm"><div>Type II: grafts contain a single class of multipolar neuron with oval or pyriform soma,
a short apical dendrite, and several thick processes. Soma sizes are typically large or
hypertrophied, ranging between 16 and 50 &#x003bc;m in diameter (<a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F7/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F7" rid-ob="figobch34regeneration2F7">Fig. 7</a>D).</div></li><li id="A4244" class="half_rhythm"><div>Type III: grafts have intermediate characteristics. In addition to the neuronal
phenotypes found in the first group, one-third of the neurons have large somas (30-32
&#x003bc;m in diameter). Interestingly, whereas type I and III graft neurons respond
to visual stimuli (see below), type II graft neurons do not, displaying only highly
synchronized, burst-like spontaneous discharges (Fig. 10). It remains to be clarified
whether unresponsiveness is linked to abnormal neuron morphology or lack of input(s), or
both (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.81">81</a>).</div></li></ul></div><div id="ch34regeneration2.Neurons_within_the_T"><h2 id="_ch34regeneration2_Neurons_within_the_T_">Neurons within the Transplant Can Be Driven by Host Eye Visual Stimulation</h2><p>What we learned from the above-mentioned and other histological studies is that fetal
tissue blocks grafted in a mature brain will never develop the specific architecture of the
normal tissue that they replace. They lack continuity with the host tissue, intrinsic
laminar organization, and neuronal arrangement in columns. Structural disorganization,
however, does not prevent the formation of synapses able to excite grafted neurons (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.69">69</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.82">82-86</a>).
Girman and Golovina (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.87">87</a>) provided indisputable
evidence that both transplanted tectal and cortical neurons can respond to visual stimuli
presented to the adult host eye.</p><div id="ch34regeneration2.Tectal_Graft_Respons"><h3>Tectal Graft Responsiveness</h3><p>Girman (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.71">71</a>) reported good visual
activity in about half of the tectal implants. Spontaneously active at rest, single-units
respond to flashing light spots as well as to stationary and manually moved targets (5-16
degrees in diameter) with circular receptive fields (RFs). Best responses are obtained
with small (3-5 degrees in diameter) black disks moved on a white background. Some units
(29%) are direction selective. Response latencies to flashing spots (<a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F8/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F8" rid-ob="figobch34regeneration2F8">Fig. 8</a>) are in the
normal range. Tactile and auditory stimuli are ineffectual. No visual response can be
recorded in cortical tissue grafts placed at the tectal level.</p><div class="iconblock whole_rhythm clearfix ten_col fig" id="figch34regeneration2F8" co-legend-rid="figlgndch34regeneration2F8"><a href="/books/NBK11505/figure/ch34regeneration2.F8/?report=objectonly" target="object" title="Figure 8" class="img_link icnblk_img figpopup" rid-figpopup="figch34regeneration2F8" rid-ob="figobch34regeneration2F8"><img class="small-thumb" src="/books/NBK11505/bin/regeneration2f8.gif" src-large="/books/NBK11505/bin/regeneration2f8.jpg" alt="Figure 8. Neuronal discharges in visually responsive (A) and unresponsive (B) tectal grafts in response to light flashes (s)." /></a><div class="icnblk_cntnt" id="figlgndch34regeneration2F8"><h4 id="ch34regeneration2.F8"><a href="/books/NBK11505/figure/ch34regeneration2.F8/?report=objectonly" target="object" rid-ob="figobch34regeneration2F8">Figure 8</a></h4><p class="float-caption no_bottom_margin">Neuronal discharges in visually responsive (A) and unresponsive (B) tectal
grafts in response to light flashes (s). PSTH for 30 presentations. E, excitatory phase;
I, inhibitory phase. Time bin: 1 ms. Redrawn from Girman (71). C, stimulating
electrodes <a href="/books/NBK11505/figure/ch34regeneration2.F8/?report=objectonly" target="object" rid-ob="figobch34regeneration2F8">(more...)</a></p></div></div></div><div id="ch34regeneration2.Cortical_Graft_Respo"><h3>Cortical Graft Responsiveness</h3><p>Both field potential (FP) and single-unit recordings have been done in types I and III
cortical grafts. FPs in grafts always consist of a negative/positive component. Wave onset
and peak have normal latencies (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.66">66</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.87">87-89</a>).
However, it is interesting to note that none of the FPs undergo polarity reversal with
depth, as occus in the normal rat primary visual cortex (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.90">90</a>), and peak amplitudes
correlate with the density of afferents (<a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F9/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F9" rid-ob="figobch34regeneration2F9">Fig. 9</a> and <a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F10/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F10" rid-ob="figobch34regeneration2F10">Fig. 10</a>).</p><div class="iconblock whole_rhythm clearfix ten_col fig" id="figch34regeneration2F9" co-legend-rid="figlgndch34regeneration2F9"><a href="/books/NBK11505/figure/ch34regeneration2.F9/?report=objectonly" target="object" title="Figure 9" class="img_link icnblk_img figpopup" rid-figpopup="figch34regeneration2F9" rid-ob="figobch34regeneration2F9"><img class="small-thumb" src="/books/NBK11505/bin/regeneration2f9.gif" src-large="/books/NBK11505/bin/regeneration2f9.jpg" alt="Figure 9. A, field potential mapping in a large occipital tissue graft." /></a><div class="icnblk_cntnt" id="figlgndch34regeneration2F9"><h4 id="ch34regeneration2.F9"><a href="/books/NBK11505/figure/ch34regeneration2.F9/?report=objectonly" target="object" rid-ob="figobch34regeneration2F9">Figure 9</a></h4><p class="float-caption no_bottom_margin">A, field potential mapping in a large occipital tissue graft. Low responses
are from the medial yellowish area devoid of thalamic afferents (see Fig. 10). Note the
wave reversal with depth (400 <i>versus</i> 100 &#x003bc;m) in the
adjacent host cortex (point <a href="/books/NBK11505/figure/ch34regeneration2.F9/?report=objectonly" target="object" rid-ob="figobch34regeneration2F9">(more...)</a></p></div></div><div class="iconblock whole_rhythm clearfix ten_col fig" id="figch34regeneration2F10" co-legend-rid="figlgndch34regeneration2F10"><a href="/books/NBK11505/figure/ch34regeneration2.F10/?report=objectonly" target="object" title="Figure 10" class="img_link icnblk_img figpopup" rid-figpopup="figch34regeneration2F10" rid-ob="figobch34regeneration2F10"><img class="small-thumb" src="/books/NBK11505/bin/regeneration2f10.gif" src-large="/books/NBK11505/bin/regeneration2f10.jpg" alt="Figure 10. Thalamic input to the preceeding graft (see Fig." /></a><div class="icnblk_cntnt" id="figlgndch34regeneration2F10"><h4 id="ch34regeneration2.F10"><a href="/books/NBK11505/figure/ch34regeneration2.F10/?report=objectonly" target="object" rid-ob="figobch34regeneration2F10">Figure 10</a></h4><p class="float-caption no_bottom_margin">Thalamic input to the preceeding graft (see Fig. 9A) is restricted to the
most responsive area. A, biotinylated dextran amine (BDA) injection confined mostly to
the LP nucleus (dotted line, lower inset). Strong projections are present in the host
cortex <a href="/books/NBK11505/figure/ch34regeneration2.F10/?report=objectonly" target="object" rid-ob="figobch34regeneration2F10">(more...)</a></p></div></div><p>Although recording field potentials is useful for delineating the graft outer limits and
the most active zones within the graft for tracer injections, field potentials do not mean
that these neurons can actually partake in any visual operation. Girman and Golovina
(<a class="bk_pop" href="#ch34regeneration2.EXTYLES.87">87</a>), however, showed, at
the single-unit level, that many graft neurons did respond to visual stimuli.
Approximately 84% of the spontaneously active neurons in type I grafts have well-defined
RFs (5-20 degrees in diameter; <a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F11/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F11" rid-ob="figobch34regeneration2F11">Fig. 11</a>) and exhibit clear responses for
either moving or stationary stimuli. Cells preferring the same stimulus seem to be in
clusters. Flashing light spots typically evoke a biphasic excitatory/inhibitory response
of 36-62 ms latency, followed by a second excitatory discharge. Movement-sensitive neurons
fire weakly, or not at all, to light spots. Most of them show clear direction selectivity
and orientation specificity. A few active neurons (16.5%) can be driven by stimulation of
either eye, the contralateral stimulation being dominant. Visually driven neurons are less
frequently encountered in type III grafts. These neurons have larger RFs (20-30 degrees)
and react only to light spots after a long delay (100-250 ms).</p><div class="iconblock whole_rhythm clearfix ten_col fig" id="figch34regeneration2F11" co-legend-rid="figlgndch34regeneration2F11"><a href="/books/NBK11505/figure/ch34regeneration2.F11/?report=objectonly" target="object" title="Figure 11" class="img_link icnblk_img figpopup" rid-figpopup="figch34regeneration2F11" rid-ob="figobch34regeneration2F11"><img class="small-thumb" src="/books/NBK11505/bin/regeneration2f11.gif" src-large="/books/NBK11505/bin/regeneration2f11.jpg" alt="Figure 11. Upper row: autocorrelograms of spontaneous neuronal activity." /></a><div class="icnblk_cntnt" id="figlgndch34regeneration2F11"><h4 id="ch34regeneration2.F11"><a href="/books/NBK11505/figure/ch34regeneration2.F11/?report=objectonly" target="object" rid-ob="figobch34regeneration2F11">Figure 11</a></h4><p class="float-caption no_bottom_margin">Upper row: autocorrelograms of spontaneous neuronal activity. A, in visually
responsive grafts (desynchronized regular pattern). As in the intact visual cortex
(94), the spike rate
increases with the recording depth. B, in unresponsive grafts (periodic <a href="/books/NBK11505/figure/ch34regeneration2.F11/?report=objectonly" target="object" rid-ob="figobch34regeneration2F11">(more...)</a></p></div></div><p>Finally, graft neurons also fire in response to electrical stimulation (10-50
&#x003bc;A) of either the host ipsilateral DLG nucleus or the contralateral visual
cortex. An important finding, suggestive of some form of topographic organization between
the DLG and the cortical graft, is that small displacements (200 &#x003bc;m) of the
stimulating electrode from the optimal geniculate site lead to a decrease or a complete
loss of response.</p></div><div id="ch34regeneration2.Are_Responses_from_t"><h3>Are Responses from the Graft Retinotopically Ordered?</h3><p>To a degree, they are. The same studies by Girman and Golovina (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.87">87</a>) indicate that large (3 mm in diameter),
highly responsive cortical grafts contain an ordered representation of the contralateral
visual field, at least of its central part, which projects normally onto area 17. First,
neurons recorded simultaneously at a given electrode position have roughly the same RF
location. Second, there is no change in RF position with depth during a single
penetration. Third, ordered changes in the recording positions on the graft surface induce
concomitant changes in the RF locations. Fourth, the orientation of the visual field
projection onto the graft appears normal relative to the skull landmarks (<a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F12/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F12" rid-ob="figobch34regeneration2F12">Fig.
12</a>). A rough retinotopic order is also observed in large, type III grafts. The
larger the grafts, the better the visual field projection: small grafts contain only a
non-ordered representation of a restricted part (20-30 degrees wide) of the nasal visual
field. Visual map order and neuron properties remain unchanged up to at least 10 months
after grafting. This is a logical result in view of the fact that long-term survival (2
years <i>in situ</i>) does not significantly affect the basic morphological
features of cortical grafts (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.91">91</a>).</p><div class="iconblock whole_rhythm clearfix ten_col fig" id="figch34regeneration2F12" co-legend-rid="figlgndch34regeneration2F12"><a href="/books/NBK11505/figure/ch34regeneration2.F12/?report=objectonly" target="object" title="Figure 12" class="img_link icnblk_img figpopup" rid-figpopup="figch34regeneration2F12" rid-ob="figobch34regeneration2F12"><img class="small-thumb" src="/books/NBK11505/bin/regeneration2f12.gif" src-large="/books/NBK11505/bin/regeneration2f12.jpg" alt="Figure 12. Near-normal visuotopic projections in type I graft placed in the right primary visual area (Oc1/V1) of an adult rat." /></a><div class="icnblk_cntnt" id="figlgndch34regeneration2F12"><h4 id="ch34regeneration2.F12"><a href="/books/NBK11505/figure/ch34regeneration2.F12/?report=objectonly" target="object" rid-ob="figobch34regeneration2F12">Figure 12</a></h4><p class="float-caption no_bottom_margin">Near-normal visuotopic projections in type I graft placed in the right
primary visual area (Oc1/V1) of an adult rat. A, recording loci at graft level (grayish
inset). Dorsal view. Graft is centered approximately 8 mm caudal to bregma and 4 mm
lateral <a href="/books/NBK11505/figure/ch34regeneration2.F12/?report=objectonly" target="object" rid-ob="figobch34regeneration2F12">(more...)</a></p></div></div></div></div><div id="ch34regeneration2.Do_Grafts_Receive_Ex"><h2 id="_ch34regeneration2_Do_Grafts_Receive_Ex_">Do Grafts Receive Extensive Afferents?</h2><p>By this point, it seems evident that under some highly controlled and replicable
experimental conditions, allogeneic fetal tissue grafts implanted at homotopic positions in
the visual brain can respond to visual stimulation of the host eye. Some cells from the
graft perform rather complex operations of visual driven signals, just like the SC and area
17 in the normal rat (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.92">92-95</a>).
The graft can resume at least a partial, ordered map of the visual field, a prerequisite for
recovery of function. However, topographic visual field representation on a graft is likely
to involve many more regenerated host afferents than the few, randomly branching fibers
reportedly able to generate light flash responses in the PN graft paradigm (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.96">96-98</a>).
Direction selectivity, orientation specificity, and binocular activation imply sophisticated
synaptic input to graft neurons (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.99">99</a>). The next question, then, is whether homologous fetal grafts in the adult
primary visual cortex receive extensive input from appropriate brain areas.</p><div id="ch34regeneration2.Tectal_Graft_Connect"><h3>Tectal Graft Connectivity</h3><p>The actual substrate of the visual responses recorded in tectal grafts is a puzzling,
still unsolved problem. Receptive field properties, latency values, and ordered
organization together suggest the presence of direct, widely distributed host retinal
input to the grafts. However, the early studies in neonate hosts showed that retinal
afferents never filled the transplants and were restricted to discrete, fiber-free
patches. Within these patches, the density of optic terminals was nearly equivalent to
that seen in the stratum griseum superficiale of normal rats. By electron microscopy,
these terminals made asymmetric (excitatory) contacts onto small, post-synaptic profiles,
many of which were dendritic spines (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.75">75</a>). However, in striking contrast with
Girman's findings, neither visually (light flash and moving disk) nor electrically (optic
nerve stimulation) evoked activity were obtained from these grafts (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.100">100</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.101">101</a>).
Only a minor fraction of the tested units could be excited orthodromically from the
ipsilateral visual cortex, the major source of graft input in these preparations (<a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F8/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F8" rid-ob="figobch34regeneration2F8">Fig. 8</a>). The failure to record retinal
activity in the latter experiments could be attributable to the low number of electrode
tracks.</p><p>Tectal tissue grafts implanted in juvenile (P15/P18) and adult hosts with the same
technical approach also display discrete "fiber-free" patches dispersed dorsally within
the fiber-rich core. However, no definitive projections from the host brain have been
identified (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.67">67</a>), and retinal
innervation to the patches remains a matter of debate (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.67">67</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.73">73</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.102">102</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.103">103</a>).
In short, there is yet very little anatomical evidence for the visual responsiveness
recorded in tectal grafts. As suggested earlier by Golden et al. (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.100">100</a>), a possible reason
for this discrepancy may be the grafting technique. Although grafts done by Golden et al.
(<a class="bk_pop" href="#ch34regeneration2.EXTYLES.100">100</a>) consist of partly
dissociated cells injected onto the surface of the SC, the transplants done by Girman
consist of "solid sheets of embryonic tectal tissue laid in the appropriate dorsoventral
orientation over the SC surface devoid of superficial laminae". In neonates, a similar
paradigm as used by Girman leads to the formation of a single, densely innervated
retinorecipient lamina covering a large part of the graft surface (<a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F6/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F6" rid-ob="figobch34regeneration2F6">Fig. 6</a>) (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.75">75</a>). Up to now, neither the connectivity nor
the neurofibrillar structure of such tectal implants in adult hosts have been studied.</p></div><div id="ch34regeneration2.Host_Afferents_to_Co"><h3>Host Afferents to Cortical Grafts</h3><p>As the electrophysiological data suggest, there should be a strong relationship between
graft responsiveness and the presence of regenerating axons (or collateral sprouts) from
ipsilateral DLG neurons. Indeed, retrograde tracers injected in type I grafts label high
numbers of DLG neurons (one-third of which projected initially to the lesioned cortical
site), whereas similar injections in type II grafts produce no labeling at all (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.81">81</a>). Whether direct DLG
input alone can account for graft visual responsiveness is, however, very unlikely,
because some type I grafts receive only extra-geniculate, and no direct geniculate,
inputs.</p></div><div id="ch34regeneration2.Major_Graft_Input_Or"><h3>Major Graft Input Originates in Host Layer 5-6</h3><p>After retrograde tracer (CTB, cholera toxin, b subunit) injection into types I-III
grafts, Gaillard and colleagues (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.66">66</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.88">88</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.89">89</a>)
saw a diversity of afferents. These afferents (always in very low number; Fig. 17) appear
in visual-related brain structures ipsilateral to the graft. The densest labeling (55-90%)
is observed in the isocortex, mostly in the occipital areas surrounding the graft (see
also Galick et al. (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.104">104</a>) and Schultz et al.
(<a class="bk_pop" href="#ch34regeneration2.EXTYLES.78">78</a>)). Together, neurons
in claustrum, periallocortical areas, and various non-visual subcortical nuclei account
for some 20% of the graft input. As expected, labeling in dorsal thalamus is highly
variable. Although practically absent in one-half of the subjects, it represents 10-30% of
all the graft afferents in the other one-half. DLG input never exceeds 10% of the total
graft input. Orbital (VO/VLO), motor (Fr2), and brainstem structures (such as the basal
nucleus of Meynert, locus coeruleus, and dorsal raphe), all projecting to the normal
visual cortex (<a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F12/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F12" rid-ob="figobch34regeneration2F12">Fig. 12</a>), are never
labeled (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.33">33</a>). Labeling in
the hemisphere opposite to the graft is always negligible.</p><p>Apart from the isocortical area, most labeled neurons (91%) are confined to the
infragranular layers (<a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F13/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F13" rid-ob="figobch34regeneration2F13">Fig. 13</a> and <a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F14/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F14" rid-ob="figobch34regeneration2F14">Fig. 14</a>),
noticeably layer 6 and sublayer 6b, close to the white matter. Layer 6b neurons in normal
adult rodents exhibit diverse cell body morphologies (<a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F14/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F14" rid-ob="figobch34regeneration2F14">Fig. 14</a> and <a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F15/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F15" rid-ob="figobch34regeneration2F15">Fig. 15</a>) and have
widespread terminal arborizations (&#x0003e;3-4 mm) in superficial cortical layers (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.105">105</a>). They appear to be
remnants of subplate neurons (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.106">106-108</a>),
which have pivotal functions during early cortical development, for instance in guiding
thalamic fibers to their appropriate cortical target area (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.109">109-111</a>)
and in governing the functional maturation of connections between DLG axons and layer 4
neurons (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.112">112</a>). They are also
involved in coordinating ocular dominance column formation (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.113">113</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.114">114</a>).
In the adult cat, subplate (white matter) and pyramidal cells of the normal and inverted
types in the infragranular cortical layers support long-range, tangential connections
(<a class="bk_pop" href="#ch34regeneration2.EXTYLES.115">115</a>).</p><div class="iconblock whole_rhythm clearfix ten_col fig" id="figch34regeneration2F13" co-legend-rid="figlgndch34regeneration2F13"><a href="/books/NBK11505/figure/ch34regeneration2.F13/?report=objectonly" target="object" title="Figure 13" class="img_link icnblk_img figpopup" rid-figpopup="figch34regeneration2F13" rid-ob="figobch34regeneration2F13"><img class="small-thumb" src="/books/NBK11505/bin/regeneration2f13.gif" src-large="/books/NBK11505/bin/regeneration2f13.jpg" alt="Figure 13. Representative labeling of projection neurons (arrows) in the host cortex (Cx) after injection of a retrograde tracer (CTb; cholera toxin, b-subunit) in a visually responsive graft (Tr)." /></a><div class="icnblk_cntnt" id="figlgndch34regeneration2F13"><h4 id="ch34regeneration2.F13"><a href="/books/NBK11505/figure/ch34regeneration2.F13/?report=objectonly" target="object" rid-ob="figobch34regeneration2F13">Figure 13</a></h4><p class="float-caption no_bottom_margin">Representative labeling of projection neurons (arrows) in the host cortex
(Cx) after injection of a retrograde tracer (CTb; cholera toxin, b-subunit) in a
visually responsive graft (Tr). Note their location in layer 6, close to the white
matter (w.m.). <a href="/books/NBK11505/figure/ch34regeneration2.F13/?report=objectonly" target="object" rid-ob="figobch34regeneration2F13">(more...)</a></p></div></div><div class="iconblock whole_rhythm clearfix ten_col fig" id="figch34regeneration2F14" co-legend-rid="figlgndch34regeneration2F14"><a href="/books/NBK11505/figure/ch34regeneration2.F14/?report=objectonly" target="object" title="Figure 14" class="img_link icnblk_img figpopup" rid-figpopup="figch34regeneration2F14" rid-ob="figobch34regeneration2F14"><img class="small-thumb" src="/books/NBK11505/bin/regeneration2f14.gif" src-large="/books/NBK11505/bin/regeneration2f14.jpg" alt="Figure 14. A-C, gallery of retrogradely labeled layer 5 pyramidal cells after CTb injection into three different responsive grafts." /></a><div class="icnblk_cntnt" id="figlgndch34regeneration2F14"><h4 id="ch34regeneration2.F14"><a href="/books/NBK11505/figure/ch34regeneration2.F14/?report=objectonly" target="object" rid-ob="figobch34regeneration2F14">Figure 14</a></h4><p class="float-caption no_bottom_margin">A-C, gallery of retrogradely labeled layer 5 pyramidal cells after CTb
injection into three different responsive grafts. Arrowheads indicate axons. All cells
are located 400-500 &#x003bc;m from the graft boundary. Scale bars, 13
&#x003bc;m. D-G, gallery <a href="/books/NBK11505/figure/ch34regeneration2.F14/?report=objectonly" target="object" rid-ob="figobch34regeneration2F14">(more...)</a></p></div></div><div class="iconblock whole_rhythm clearfix ten_col fig" id="figch34regeneration2F15" co-legend-rid="figlgndch34regeneration2F15"><a href="/books/NBK11505/figure/ch34regeneration2.F15/?report=objectonly" target="object" title="Figure 15" class="img_link icnblk_img figpopup" rid-figpopup="figch34regeneration2F15" rid-ob="figobch34regeneration2F15"><img class="small-thumb" src="/books/NBK11505/bin/regeneration2f15.gif" src-large="/books/NBK11505/bin/regeneration2f15.jpg" alt="Figure 15. Left panel: camera lucida drawings of retrogradely labeled cells in layer 6b after CTb injection into another responsive graft." /></a><div class="icnblk_cntnt" id="figlgndch34regeneration2F15"><h4 id="ch34regeneration2.F15"><a href="/books/NBK11505/figure/ch34regeneration2.F15/?report=objectonly" target="object" rid-ob="figobch34regeneration2F15">Figure 15</a></h4><p class="float-caption no_bottom_margin">Left panel: camera lucida drawings of retrogradely labeled cells in layer 6b
after CTb injection into another responsive graft. Dotted lines denote the upper limit
of the white matter (w.m.). Arrowheads indicate the location and the distance of the
graft. <a href="/books/NBK11505/figure/ch34regeneration2.F15/?report=objectonly" target="object" rid-ob="figobch34regeneration2F15">(more...)</a></p></div></div></div><div id="ch34regeneration2.This_Pattern_Is_Spec"><h3>This Pattern Is Specified by Eye Opening</h3><p>When performed in neonate hosts, the same experiments always lead to greater density and
diversity of graft inputs (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.89">89</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.116">116</a>). At the cortical
level, for instance, frontal (Fr2; the frontal eye field in primates) and orbital (LO/VLO)
areas are moderately but systematically labeled, and the somas of the isocortical
afferents distribute about equally between layers 2-3 and 5-6. At the thalamic level,
owing to the severe (75%) atrophy of the DLG (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.117">117</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.118">118</a>),
most inputs originate in the LP/LD complex and the central intralaminar nuclei, an
unlabeled cell group in adult hosts (<a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F16/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F16" rid-ob="figobch34regeneration2F16">Fig. 16</a>).</p><div class="iconblock whole_rhythm clearfix ten_col fig" id="figch34regeneration2F16" co-legend-rid="figlgndch34regeneration2F16"><a href="/books/NBK11505/figure/ch34regeneration2.F16/?report=objectonly" target="object" title="Figure 16" class="img_link icnblk_img figpopup" rid-figpopup="figch34regeneration2F16" rid-ob="figobch34regeneration2F16"><img class="small-thumb" src="/books/NBK11505/bin/regeneration2f16.gif" src-large="/books/NBK11505/bin/regeneration2f16.jpg" alt="Figure 16. Upper row: quantitative differences (mean &#x000b1; SD) in graft input between neonates (P0) and adult (P120) recipients." /></a><div class="icnblk_cntnt" id="figlgndch34regeneration2F16"><h4 id="ch34regeneration2.F16"><a href="/books/NBK11505/figure/ch34regeneration2.F16/?report=objectonly" target="object" rid-ob="figobch34regeneration2F16">Figure 16</a></h4><p class="float-caption no_bottom_margin">Upper row: quantitative differences (mean &#x000b1; SD) in graft input
between neonates (P0) and adult (P120) recipients. A, raw number of isocortical cells.
B, proportions of cells per isocortical layer. Counts performed on half the brain of
each subject. <a href="/books/NBK11505/figure/ch34regeneration2.F16/?report=objectonly" target="object" rid-ob="figobch34regeneration2F16">(more...)</a></p></div></div><p>We conclude that the age of the recipient appears to affect both the density and the
topology of the graft afferents (for similar data with parietal grafts, see Castro et al.
(<a class="bk_pop" href="#ch34regeneration2.EXTYLES.119">119</a>) and Schultz et al
(<a class="bk_pop" href="#ch34regeneration2.EXTYLES.78">78</a>).
). Additional studies show,
moreover, that the most dramatic changes in the afferent pattern occur in the second
postnatal week, before the onset of the critical period for rat visual cortex (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.120">120</a>). Nearly all
isocortical inputs to the graft in P15 hosts originate in the infragranular layers, mostly
from layer 6, a proportion not significantly different from that found in older recipients
(<a class="bk_pop" href="#ch34regeneration2.EXTYLES.66">66</a>). This age-related
laminar shaping is a two-step process that affects all layers, but the supragranular
layers are affected more specifically. It is completed in frontal and temporal areas about
1 week earlier than in the occipital areas surrounding the graft (<a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F17/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F17" rid-ob="figobch34regeneration2F17">Fig. 17</a>). The delay
is likely related to the cortical ontogenetic program that proceeds radially (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.121">121</a>) as well as
tangentially through rostrocaudal and lateromedial directions (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.122">122</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.123">123</a>).</p><div class="iconblock whole_rhythm clearfix ten_col fig" id="figch34regeneration2F17" co-legend-rid="figlgndch34regeneration2F17"><a href="/books/NBK11505/figure/ch34regeneration2.F17/?report=objectonly" target="object" title="Figure 17" class="img_link icnblk_img figpopup" rid-figpopup="figch34regeneration2F17" rid-ob="figobch34regeneration2F17"><img class="small-thumb" src="/books/NBK11505/bin/regeneration2f17.gif" src-large="/books/NBK11505/bin/regeneration2f17.jpg" alt="Figure 17. Proportions of labeled cells (mean &#x000b1; SD) in the temporal (Te1-3) and occipital (Oc1-2M) areas as a function of the age of the host." /></a><div class="icnblk_cntnt" id="figlgndch34regeneration2F17"><h4 id="ch34regeneration2.F17"><a href="/books/NBK11505/figure/ch34regeneration2.F17/?report=objectonly" target="object" rid-ob="figobch34regeneration2F17">Figure 17</a></h4><p class="float-caption no_bottom_margin">Proportions of labeled cells (mean &#x000b1; SD) in the temporal (Te1-3)
and occipital (Oc1-2M) areas as a function of the age of the host. Note the absence of
supragranular input from temporal areas in 2-week-old recipients. Redrawn from Domballe
et <a href="/books/NBK11505/figure/ch34regeneration2.F17/?report=objectonly" target="object" rid-ob="figobch34regeneration2F17">(more...)</a></p></div></div></div><div id="ch34regeneration2.The_Potential_of_Lay"><h3>The Potential of Layer 6 Neurons to Survive Injury and to Drive Grafts</h3><p>A major outcome of all the above-mentioned studies is that afferent innervation to a
cortical graft in adult host originates mostly from a small population of layer 6 neurons
located in the immediate graft surround. Cortical layer 6 is a target for thalamic fibers.
The layer 6 neurons display all known visual response types (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.94">94</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.95">95</a>),
regardless of their morphology. Of the four layer 6 cells injected with HRP by Parnavelas
et al. (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.124">124</a>), one multipolar
cell was an "ON-OFF" cell, two pyramidal cells were "complex" cells, and the last fusiform
cell type was a "non-oriented" cell. In the absence of direct thalamic input, layer 6
neurons may thus be able to drive visual information to the graft.</p><p>Why layer 2-3 neurons do not contact the graft in adults is not understood. Among many
possibilities, one would be that these late-generated (E17-E20) corticocortical projection
neurons, which have low survival rates during development (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.125">125</a>), are very sensitive
to lesion-induced retrograde degeneration and/or deleterious changes in their environment
(but see Szele et al. (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.126">126</a>)). Conversely,
these neurons may be able to regenerate axons, but these axons do not penetrate the graft
because of negative influences from reactive astroglial elements and/or graft neurons. For
instance, <i>in vitro</i> assays (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.6">6</a>) have shown that
endogenous levels of neurotrophin-3 (NT-3) reduce axonal branching and repel layer 2-3
neurons but have opposite effects on layer 6 neurons. For some days after implantation,
the graft (which is producing NT-3) may thus be repulsive to layer 2-3 axons but
attractive to layer 6/6b neurons, which express NT-3 receptors (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.127">127</a>). Regardless of how
fascinating these latter observations are, multiple survival and growth-promoting factors
produced by the graft and the injured cortex may also allow layer 6 neuron survival and
axonal elongation. For instance, neurotrophin-4 (NT-4) is as effective as NT-3 in
increasing the length of the dendritic processes of layer 6 pyramidal cells of juvenile
ferrets (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.128">128</a>). Furthermore, layer
6b neurons have receptors to basic fibroblast growth factor (FGF-2), a critical survival
substrate for subplate neurons (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.129">129</a>). FGF-2 is
suspected to protect adult layer 6b neurons from death after lesions (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.130">130</a>) but has no survival
effect on 1-week-old, layer 2-3 callosal projection neurons (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.131">131</a>). Deciphering why
some layer 6 neurons in the adult brain have the potential for elongating their axons and
whether these neurons have excitatory phenotypes will be an interesting challenge,
especially in the context of these cells consistently labeling regardless of the grafting
strategy (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.78">78</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.132">132</a>).</p></div><div id="ch34regeneration2.Anatomical_Support_f"><h3>Anatomical Support for Topographic Order in Grafts Is Still Lacking</h3><p>Mapping studies suggest that host afferents are topically organized in large tectal and
cortical E15-17 embryonic tissue grafts. These results need anatomical confirmation,
however. Beside occasional statements (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.119">119</a>), this issue has only been specifically
addressed in a single study using neonate recipients. The triple labeling approach by
Worthington and Harvey (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.133">133</a>) shows that tectal
tissue grafts receive non-topographically organized, but nevertheless non-random,
rudimentarily ordered cortical inputs. To date, no such investigation has been carried out
with adult hosts, likely because one can hardly imagine how the discrete afferent
projections reviewed above may form a coherent visual map onto grafts (see section 2.7.3
from the previous chapter). This negative reasoning does not consider: first that map
formation may require a specific, highly controlled transplantation procedure (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.71">71</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.133">133</a>),
including possibly the correct orientation of the graft in the lesion cavity (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.134">134</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.135">135</a>); second, that
labeled graft afferents may reflect only a negligible proportion of the actual projecting
host neurons; and third, that single-unit recordings with carefully engineered
microelectrodes (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.136">136</a>) may be more
powerful than tracer injections to detect small point-to-point shifts in connectivity
between restricted brain areas. Meticulous surgical preparation, ingenious recording
conditions, and use of self-made, highly specific tungsten in glass electrodes of the
Levick's type may together account for Girman's successful recordings (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.94">94</a>). In our opinion,
unequivocal assessment of topographic host-graft projections requires further studies
combining an optimal surgical strategy, a highly sensitive fiber detection process (see
below), and a careful electrophysiological approach replicating Girman's approach.</p></div></div><div id="ch34regeneration2.Can_Grafts_Send_Affe"><h2 id="_ch34regeneration2_Can_Grafts_Send_Affe_">Can Grafts Send Afferents to Host Targets?</h2><p>In line with numerous results showing low numbers of afferents coming to the transplant, it
has been repeatedly assumed that allogeneic embryonic tissue grafts do not send long-range
projections to the adult host. Our own attempts using either biotinylated dextran amine
(BDA) or the carbocyanine dye DiI (1,1'-didodecyl-3,3,3',3'-tetramethyl-indocarbocyanine
perchlorate) as anterograde tracers confirm this assumption. This failure is commonly
attributed to growth inhibitory conditions present in the mature brain (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.14">14</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.137">137</a>).
Possible technical limitations are rarely addressed (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.138">138-141</a>).
Yet, there are some intriguing morpho-functional observations (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.84">84</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.85">85</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.142">142-148</a>),
suggesting that blocks of embryonic neurons grafted into the mature brain might not be able
to transport exogenously provided tracers beyond the graft-host transition zone. In
opposition to this, long axonal trajectories have been clearly detected in some experimental
conditions, either after pre-loading dissociated donor cells with dyes (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.149">149</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.150">150</a>) or by targeting
specific markers expressed by grafted cells (Thy-1.2 allelic system; microtubule-associated
protein MAP1x/1B) (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.151">151-155</a>).
This has been a routine procedure for xenogeneic tissue grafts (for examples, see Lund et
al. (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.156">156</a>),
Li and Raisman (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.157">157</a>), Davies et al. (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.158">158</a>), Isacson and Deacon
(<a class="bk_pop" href="#ch34regeneration2.EXTYLES.159">159</a>), and Armstrong et al.
(<a class="bk_pop" href="#ch34regeneration2.EXTYLES.18">18</a>)). A plausible
hypothesis is, then, that all fetal graft neurons, regardless of their origins, are
intrinsically capable of elongating processes when placed in a mature brain, but that
detection of these processes outside the graft structure requires a non-invasive, anatomical
approach. This hypothesis has been verified recently in occipital cortex tissue grafts
(<a class="bk_pop" href="#ch34regeneration2.EXTYLES.160">160</a>) using transgenic E15
mouse fetuses expressing a GFP protein variant under the control of a chicken beta-actin
promoter (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.161">161</a>) as donors (<a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F18/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F18" rid-ob="figobch34regeneration2F18">Fig.
18</a> and <a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F19/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F19" rid-ob="figobch34regeneration2F19">Fig. 19</a>).</p><div class="iconblock whole_rhythm clearfix ten_col fig" id="figch34regeneration2F18" co-legend-rid="figlgndch34regeneration2F18"><a href="/books/NBK11505/figure/ch34regeneration2.F18/?report=objectonly" target="object" title="Figure 18" class="img_link icnblk_img figpopup" rid-figpopup="figch34regeneration2F18" rid-ob="figobch34regeneration2F18"><img class="small-thumb" src="/books/NBK11505/bin/regeneration2f18.gif" src-large="/books/NBK11505/bin/regeneration2f18.jpg" alt="Figure 18. Dr." /></a><div class="icnblk_cntnt" id="figlgndch34regeneration2F18"><h4 id="ch34regeneration2.F18"><a href="/books/NBK11505/figure/ch34regeneration2.F18/?report=objectonly" target="object" rid-ob="figobch34regeneration2F18">Figure 18</a></h4><p class="float-caption no_bottom_margin">Dr. Okabe's eGFP-expressing neonate mice look "green" all over their body
when illuminated with an UV source. See: http://kumikae01.gen-info.osaka-u.ac.jp/tg/tg-ad.cfm. </p></div></div><div class="iconblock whole_rhythm clearfix ten_col fig" id="figch34regeneration2F19" co-legend-rid="figlgndch34regeneration2F19"><a href="/books/NBK11505/figure/ch34regeneration2.F19/?report=objectonly" target="object" title="Figure 19" class="img_link icnblk_img figpopup" rid-figpopup="figch34regeneration2F19" rid-ob="figobch34regeneration2F19"><img class="small-thumb" src="/books/NBK11505/bin/regeneration2f19.gif" src-large="/books/NBK11505/bin/regeneration2f19.jpg" alt="Figure 19. A, location of the eGFP-positive grafts at the cortical surface with respect to bregma (B = 0) after reconstruction from serial brain sections." /></a><div class="icnblk_cntnt" id="figlgndch34regeneration2F19"><h4 id="ch34regeneration2.F19"><a href="/books/NBK11505/figure/ch34regeneration2.F19/?report=objectonly" target="object" rid-ob="figobch34regeneration2F19">Figure 19</a></h4><p class="float-caption no_bottom_margin">A, location of the eGFP-positive grafts at the cortical surface with respect
to bregma (B = 0) after reconstruction from serial brain sections. B, representative
implantation (B-3.5). Darkfield microscopy. Note white matter bundles around and within
the <a href="/books/NBK11505/figure/ch34regeneration2.F19/?report=objectonly" target="object" rid-ob="figobch34regeneration2F19">(more...)</a></p></div></div><div id="ch34regeneration2.Embryonic_Cortical_T"><h3>Embryonic Cortical Tissue Allografts Have Massive Efferents</h3><p>A major finding of the above study is that despite immediate implantation, nearly all
grafts into mature (P60/P90), wild-type mice appear physically well integrated in the host
cortex (<a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F19/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F19" rid-ob="figobch34regeneration2F19">Fig. 19</a>). Moreover, they
show massive outgrowth all along their interface with the cortical parenchyma and send
extensive efferents throughout the host ipsilateral pallium, mainly to its cortical mantle
(<a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F20/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F20" rid-ob="figobch34regeneration2F20">Fig.
20</a>).</p><div class="iconblock whole_rhythm clearfix ten_col fig" id="figch34regeneration2F20" co-legend-rid="figlgndch34regeneration2F20"><a href="/books/NBK11505/figure/ch34regeneration2.F20/?report=objectonly" target="object" title="Figure 20" class="img_link icnblk_img figpopup" rid-figpopup="figch34regeneration2F20" rid-ob="figobch34regeneration2F20"><img class="small-thumb" src="/books/NBK11505/bin/regeneration2f20.gif" src-large="/books/NBK11505/bin/regeneration2f20.jpg" alt="Figure 20. Camera lucida drawings of graft projections into the ipsilateral cortex of the former case as seen at a low magnification power (&#x000d7;4)." /></a><div class="icnblk_cntnt" id="figlgndch34regeneration2F20"><h4 id="ch34regeneration2.F20"><a href="/books/NBK11505/figure/ch34regeneration2.F20/?report=objectonly" target="object" rid-ob="figobch34regeneration2F20">Figure 20</a></h4><p class="float-caption no_bottom_margin">Camera lucida drawings of graft projections into the ipsilateral cortex of
the former case as seen at a low magnification power (&#x000d7;4). Brain sections
are arranged according to their bregma level. The grayish zone in each section
corresponds to <a href="/books/NBK11505/figure/ch34regeneration2.F20/?report=objectonly" target="object" rid-ob="figobch34regeneration2F20">(more...)</a></p></div></div><p>Rostrally, graft fibers innervate a large medial sector of the brain including frontal
association (FrA), secondary motor (M2), prelimbic (PrL), anterior cingulate (Cg1-2),
medial orbital (MO), and infralimbic (IL) areas. Discrete fibers terminate within the
orbital areas VO/LO and the claustrum (CL). At the bregma level, efferents distribute from
area Cg1 medially to the somatosensory cortex laterally. Labeling extends throughout
layers 2-3 and 5-6 in motor (Fr2) and sensorimotor (HL) areas but remains in lamina 6b at
the barrel field (BF) level (<a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F21/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F21" rid-ob="figobch34regeneration2F21">Fig. 21</a> and <a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F22/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F22" rid-ob="figobch34regeneration2F22">Fig. 22</a>).</p><div class="iconblock whole_rhythm clearfix ten_col fig" id="figch34regeneration2F21" co-legend-rid="figlgndch34regeneration2F21"><a href="/books/NBK11505/figure/ch34regeneration2.F21/?report=objectonly" target="object" title="Figure 21" class="img_link icnblk_img figpopup" rid-figpopup="figch34regeneration2F21" rid-ob="figobch34regeneration2F21"><img class="small-thumb" src="/books/NBK11505/bin/regeneration2f21.gif" src-large="/books/NBK11505/bin/regeneration2f21.jpg" alt="Figure 21. Composite images showing the cortical distribution of graft efferents in HL (left) and V2L (right) areas of two different animals." /></a><div class="icnblk_cntnt" id="figlgndch34regeneration2F21"><h4 id="ch34regeneration2.F21"><a href="/books/NBK11505/figure/ch34regeneration2.F21/?report=objectonly" target="object" rid-ob="figobch34regeneration2F21">Figure 21</a></h4><p class="float-caption no_bottom_margin">Composite images showing the cortical distribution of graft efferents in HL
(left) and V2L (right) areas of two different animals. Note the high density of fibers
in layer 6. Inverted contrast from fluorescent material. Corpus callosum (CC) is
downward. <a href="/books/NBK11505/figure/ch34regeneration2.F21/?report=objectonly" target="object" rid-ob="figobch34regeneration2F21">(more...)</a></p></div></div><div class="iconblock whole_rhythm clearfix ten_col fig" id="figch34regeneration2F22" co-legend-rid="figlgndch34regeneration2F22"><a href="/books/NBK11505/figure/ch34regeneration2.F22/?report=objectonly" target="object" title="Figure 22" class="img_link icnblk_img figpopup" rid-figpopup="figch34regeneration2F22" rid-ob="figobch34regeneration2F22"><img class="small-thumb" src="/books/NBK11505/bin/regeneration2f22.gif" src-large="/books/NBK11505/bin/regeneration2f22.jpg" alt="Figure 22. Graft efferents in the caudal brain (4 mm beyond bregma)." /></a><div class="icnblk_cntnt" id="figlgndch34regeneration2F22"><h4 id="ch34regeneration2.F22"><a href="/books/NBK11505/figure/ch34regeneration2.F22/?report=objectonly" target="object" rid-ob="figobch34regeneration2F22">Figure 22</a></h4><p class="float-caption no_bottom_margin">Graft efferents in the caudal brain (4 mm beyond bregma). A, schematic
drawing (adapted from Paxinos and Franklin (175)) showing the location of the
accompanying pictures (red dots). Gray levels are representative of the fiber density.
B, efferents in <a href="/books/NBK11505/figure/ch34regeneration2.F22/?report=objectonly" target="object" rid-ob="figobch34regeneration2F22">(more...)</a></p></div></div><p>At the transplant level and beyond, labeling from the GFP donor tissue fills the host
ipsilateral cortex from the retrosplenial granular area to the lateral entorhinal region.
Efferents in V2L and Te1-2 areas are especially dense in layers 1-3, 5a, and 6. Further
caudally, labeled fibers occupy predominantly the cortical layers 5-6 as well as the
PrS/PaS hippocampic regions.</p><p>Finally, afferents with terminal-like profiles are systematically present in the
dorsomedial sector (as well as along the lateral rim) of the striatum and into the
basolateral and central amygdaloid nuclei (<a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F23/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F23" rid-ob="figobch34regeneration2F23">Fig. 23</a>). All these
structures, including the cortical areas listed above, are normal targets of the rodent
visual cortex (see <a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F2/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F2" rid-ob="figobch34regeneration2F2">Fig. 2</a>).</p><div class="iconblock whole_rhythm clearfix ten_col fig" id="figch34regeneration2F23" co-legend-rid="figlgndch34regeneration2F23"><a href="/books/NBK11505/figure/ch34regeneration2.F23/?report=objectonly" target="object" title="Figure 23" class="img_link icnblk_img figpopup" rid-figpopup="figch34regeneration2F23" rid-ob="figobch34regeneration2F23"><img class="small-thumb" src="/books/NBK11505/bin/regeneration2f23.gif" src-large="/books/NBK11505/bin/regeneration2f23.jpg" alt="Figure 23. Graft efferents in the striatum and the amygdala." /></a><div class="icnblk_cntnt" id="figlgndch34regeneration2F23"><h4 id="ch34regeneration2.F23"><a href="/books/NBK11505/figure/ch34regeneration2.F23/?report=objectonly" target="object" rid-ob="figobch34regeneration2F23">Figure 23</a></h4><p class="float-caption no_bottom_margin">Graft efferents in the striatum and the amygdala. Fluorescence microscopy.
A, labeling in the dorsomedial striatum, below area Fr1 (B+1.2). Scale bar, 100
&#x003bc;m. B and C, labeling in the amygdala, laterodorsal nucleus (B+1.0). Scale
bars, 150 and <a href="/books/NBK11505/figure/ch34regeneration2.F23/?report=objectonly" target="object" rid-ob="figobch34regeneration2F23">(more...)</a></p></div></div><p>Although always disrupted by surgery (<a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F19/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F19" rid-ob="figobch34regeneration2F19">Fig. 19</a> and <a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F27/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F27" rid-ob="figobch34regeneration2F27">Fig. 27</a>), the white matter (external capsule
and corpus callosum) never appears to provide an attractive substrate for graft efferents.
Even at the exit point from the graft, outgrowing fibers always appear to prefer
elongating through the deep gray matter (layer 6) of the cortex, the major pathway for
long distance, intrahemispheric corticocortical axons in rodents (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.162">162</a>) (<a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F24/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F24" rid-ob="figobch34regeneration2F24">Fig.
24</a>).</p><div class="iconblock whole_rhythm clearfix ten_col fig" id="figch34regeneration2F27" co-legend-rid="figlgndch34regeneration2F27"><a href="/books/NBK11505/figure/ch34regeneration2.F27/?report=objectonly" target="object" title="Figure 27" class="img_link icnblk_img figpopup" rid-figpopup="figch34regeneration2F27" rid-ob="figobch34regeneration2F27"><img class="small-thumb" src="/books/NBK11505/bin/regeneration2f27.gif" src-large="/books/NBK11505/bin/regeneration2f27.jpg" alt="Figure 27. Destruction of the underlying white matter (arrows) allows graft efferents to invade the hippocampus (B-3." /></a><div class="icnblk_cntnt" id="figlgndch34regeneration2F27"><h4 id="ch34regeneration2.F27"><a href="/books/NBK11505/figure/ch34regeneration2.F27/?report=objectonly" target="object" rid-ob="figobch34regeneration2F27">Figure 27</a></h4><p class="float-caption no_bottom_margin">Destruction of the underlying white matter (arrows) allows graft efferents
to invade the hippocampus (B-3.6). Darkfield microscopy. Cx, host cortex; DG, dentate
gyrus; Hip, hippocampus; Tr, transplant; Sub, subiculum; w.m., white matter. </p></div></div><div class="iconblock whole_rhythm clearfix ten_col fig" id="figch34regeneration2F24" co-legend-rid="figlgndch34regeneration2F24"><a href="/books/NBK11505/figure/ch34regeneration2.F24/?report=objectonly" target="object" title="Figure 24" class="img_link icnblk_img figpopup" rid-figpopup="figch34regeneration2F24" rid-ob="figobch34regeneration2F24"><img class="small-thumb" src="/books/NBK11505/bin/regeneration2f24.gif" src-large="/books/NBK11505/bin/regeneration2f24.jpg" alt="Figure 24. Fiber outgrowth from a small (0." /></a><div class="icnblk_cntnt" id="figlgndch34regeneration2F24"><h4 id="ch34regeneration2.F24"><a href="/books/NBK11505/figure/ch34regeneration2.F24/?report=objectonly" target="object" rid-ob="figobch34regeneration2F24">Figure 24</a></h4><p class="float-caption no_bottom_margin">Fiber outgrowth from a small (0.5 mm<sup>2</sup>) transplant centered 2 mm
caudal to bregma within the lateral parietal association (LptA) area. Outgrowth occurs
throughout the graft-cortex junction (V2L area). More laterally (S1 area), fibers
display obvious preference <a href="/books/NBK11505/figure/ch34regeneration2.F24/?report=objectonly" target="object" rid-ob="figobch34regeneration2F24">(more...)</a></p></div></div><p>Very few fibers can, therefore, extend to subcortical visual targets and the opposite
hemisphere. Terminal-like arrangements can nevertheless be detected in the dorsal visual
thalamus (Rt, LP/LD, DLG, Po), the pretectum (APT), SC, and even in the lateral division
of the pontine nuclei (Pn; <a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F22/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F22" rid-ob="figobch34regeneration2F22">Fig.
22</a>), the ultimate target of the rodent visual cortex (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.39">39</a>) (<a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F25/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F25" rid-ob="figobch34regeneration2F25">Fig.
25</a> and <a class="figpopup" href="/books/NBK11505/figure/ch34regeneration2.F26/?report=objectonly" target="object" rid-figpopup="figch34regeneration2F26" rid-ob="figobch34regeneration2F26">Fig. 26</a>).</p><div class="iconblock whole_rhythm clearfix ten_col fig" id="figch34regeneration2F25" co-legend-rid="figlgndch34regeneration2F25"><a href="/books/NBK11505/figure/ch34regeneration2.F25/?report=objectonly" target="object" title="Figure 25" class="img_link icnblk_img figpopup" rid-figpopup="figch34regeneration2F25" rid-ob="figobch34regeneration2F25"><img class="small-thumb" src="/books/NBK11505/bin/regeneration2f25.gif" src-large="/books/NBK11505/bin/regeneration2f25.jpg" alt="Figure 25. Graft efferents into the corpus callosum (CC)." /></a><div class="icnblk_cntnt" id="figlgndch34regeneration2F25"><h4 id="ch34regeneration2.F25"><a href="/books/NBK11505/figure/ch34regeneration2.F25/?report=objectonly" target="object" rid-ob="figobch34regeneration2F25">Figure 25</a></h4><p class="float-caption no_bottom_margin">Graft efferents into the corpus callosum (CC). All pictures are taken
between the cingulate bundle (cg) and the brain midline. Fluorescence microscopy from
Alexa-fluor-treated material. A, callosal fibers are rare at this brain level (B-1.7).
Note the <a href="/books/NBK11505/figure/ch34regeneration2.F25/?report=objectonly" target="object" rid-ob="figobch34regeneration2F25">(more...)</a></p></div></div><div class="iconblock whole_rhythm clearfix ten_col fig" id="figch34regeneration2F26" co-legend-rid="figlgndch34regeneration2F26"><a href="/books/NBK11505/figure/ch34regeneration2.F26/?report=objectonly" target="object" title="Figure 26" class="img_link icnblk_img figpopup" rid-figpopup="figch34regeneration2F26" rid-ob="figobch34regeneration2F26"><img class="small-thumb" src="/books/NBK11505/bin/regeneration2f26.gif" src-large="/books/NBK11505/bin/regeneration2f26.jpg" alt="Figure 26. Single graft fiber elongating in the internal capsule to zona incerta, a normal subthalamic target of the occipital cortex." /></a><div class="icnblk_cntnt" id="figlgndch34regeneration2F26"><h4 id="ch34regeneration2.F26"><a href="/books/NBK11505/figure/ch34regeneration2.F26/?report=objectonly" target="object" rid-ob="figobch34regeneration2F26">Figure 26</a></h4><p class="float-caption no_bottom_margin">Single graft fiber elongating in the internal capsule to zona incerta, a
normal subthalamic target of the occipital cortex. Terminal fields are never seen in
this region. Fluorescence microscopy. Scale bar, 150 &#x003bc;m. Upper inset,
enlargement of <a href="/books/NBK11505/figure/ch34regeneration2.F26/?report=objectonly" target="object" rid-ob="figobch34regeneration2F26">(more...)</a></p></div></div></div><div id="ch34regeneration2.Implications_for_Fut"><h3>Implications for Future Research</h3><p>Besides the unequivocal demonstration that developing and regenerating fetal allograft
neurons possess a strong capacity for extending axons over considerable distances in the
mature host brain parenchyma, the results deserve further comments. First, allowing a
delay between tissue sampling and implantation is clearly not necessary for outgrowth.
Using a similar surgical protocol, extensive outgrowth can be achieved with cortical
frontal and substantia nigra tissue grafts (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.64">64</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.163">163</a>). For instance, 11
days after grafting, frontal graft growth cone-like figures end up in the cerebral
peduncle. Second, the massive fiber outgrowth taking place along the graft-host parenchyma
interface argues against the current suggestion that lesion-induced glial scar formation
and local overexpression of repulsive molecules (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.137">137</a>) impede neurite
growth <i>in vivo</i>. Third, most outgrowing axons follow a normal route in the
brain parenchyma and terminate in normal target fields, indicating that cues for correct
axonal guidance are readily present in the mature brain (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.159">159</a>, <a class="bk_pop" href="#ch34regeneration2.EXTYLES.164">164</a>).
However, some outgrowing axons spread into inappropriate targets. Fibers and terminal
fields have been detected at considerable distances from the graft locus in the acumbens
area, olfactory peduncle, tenia tecta, and PBg nucleus, raising again the question of the
specificity of innervation (see section 2.4 from the previous chapter).
Non-target-directed elongation in the mature brain has already been reported for olfactory
bulb neurons transplanted ectopically into the frontal cortex (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.152">152</a>). Fourth and
finally, adult white matter appears to be an insurmountable obstacle for most developing
axons in view that graft fibers grow clearly less through white matter tracts than through
infragranular cortical gray layers. In addition, accidental removal of the white matter
during surgery allows graft efferents to invade the underlying hippocampic structures
(neuropil layers, dentate gyrus, and subiculum).</p><p>Neurite growth inhibition by myelin is currently (but not exclusively (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.165">165</a>)) explained by
interactions between myelin-related inhibitory factors (Nogo-A protein; myelin-associated
glycoprotein, MAG; and oligodendrocytes-myelin glycoprotein, OMgp) and a common neuronal
Nogo receptor (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.166">166-168</a>). Whether such
inhibitory interactions make for graft axon repulsion in graft situations is debatable, in
part because the neuronal Nogo receptor seems barely detectable in the normal brain, at
least until the end of the first postnatal week (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.169">169</a>). The implication is
that graft axons would be able to navigate for some 2 weeks in white matter tracts before
being stopped by inhibitory ligands. This is clearly not what we saw.</p></div></div><div id="ch34regeneration2.Restoration_of_Visua"><h2 id="_ch34regeneration2_Restoration_of_Visua_">Restoration of Visual Behavior</h2><p>Only a few behavioral studies have investigated whether fetal tectal or occipital grafts
can mediate recovery of impaired visual function in adult rats. Results are inconsistent.
Stein et al. (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.170">170</a>) transplanted frontal
and occipital E18-19 tissue blocks into bilateral aspirated occipital cortices and then
trained subjects (albino rats) on both a brightness (neutral-grey levels) and a pattern
(oblique stripes) discrimination task. Rats with frontal tissue grafts can learn the
brightness task more rapidly and more accurately than animals with lesions alone. Occipital
tissue grafts are inefficient. None of the grafted subjects can solve the pattern
discrimination problem. In no case can graft efferents be clearly identified following HRP
tracing methods. In a later work, Stein and Mufson (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.171">171</a>) obtained equally good
results in both types of transplants in solving both tasks after pretreatment of the
recipients (pigmented rats) with cyclosporin A. How these experimental modifications might
affect the performance of rats having occipital tissue grafts is not discussed in this
study. The puzzling effect of the frontal grafts is attributed to the release of specific
(but unknown) recovery-promoting factors able to spare some residual visual circuits in the
host brain. Some studies emphasize, however, that sparing of function is possible only with
homotopic grafts (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.172">172</a>), and that heterotopic
transplants cannot form viable synapses with the host tissue (<a class="bk_pop" href="#ch34regeneration2.EXTYLES.173">173</a>). Clearly, the
behavioral performance of adult subjects with occipital grafts needs closer examination.</p></div><div id="ch34regeneration2.AFN1"><h2 id="_ch34regeneration2_AFN1_">About the Authors</h2><p>
<div class="graphic"><img src="/books/NBK11505/bin/regeneration1fu2.jpg" alt="Image regeneration1fu2.jpg" /></div>
University of Poitiers, where he received his B.Sc. (1969) and his M.Sc. (1971) in
physiology. He then obtained a Ph.D. (1975) and a Doctorates-Sciences (1984) in
neurophysiology. Until recently, most of his studies focused on aspects of binocular
information processing in the amphibian visual system, mainly on the functional
properties of the crossed isthmo-tectal pathway. He is now examining host-graft
relationships in the adult mammalian visual system. Since 1977, Dr. Gaillard has been a
senior investigator (Charge de recherches) of the Centre National de la Recherche
Scientifique (CNRS) at the Institut de Physiologie et Biologie Cellulaires (UMR 6187),
Poitiers, France.</p><p>
<div class="graphic"><img src="/books/NBK11505/bin/regeneration1fu1.jpg" alt="Image regeneration1fu1.jpg" /></div>
Dr. Yves Sauve was born in Montreal, Canada. He attended the University
of Montreal where he received his B.Sc. in Biochemistry in 1983 and his M.Sc. in
Neuroscience in 1988 with Dr. Thomas Reader, focusing on the neurochemistry of
catecholamines and their receptors in the CNS. He then obtained his Ph.D. in Physiology
under Dr. Michael Rasminsky at McGill University in 1995, where his research focused on
the electrophysiological evaluation of reformed synapses between regenerating RGC axons
and neurons in the superior colliculus, using the preparation developed in Dr. Albert
Aguayo's group. Dr. Sauve subsequently undertook postdoctoral studies with Dr. Raymond
Lund at the Institute of Ophthalmology (University College London), where he developed
electrophysiological approaches to evaluate visual responsiveness in rodent models of
retinal degeneration. In 2001, he became assistant professor of Ophthalmology and Visual
Sciences at the Moran Eye Center (University of Utah), where he is currently evaluating
rod and cone function following retinal degeneration, transplant therapies, and
regeneration in the adult mammalian visual pathways.</p></div><div id="ch34regeneration2.References"><h2 id="_ch34regeneration2_References_">References</h2><dl class="temp-labeled-list"><dt>1.</dt><dd><div class="bk_ref" id="ch34regeneration2.EXTYLES.1">Zihl J. Localised CNS lesions and their effect on visual function. 2000. </div></dd><dt>2.</dt><dd><div class="bk_ref" id="ch34regeneration2.EXTYLES.2">Chen DF, Jhaveri S, Schneider GE. Intrinsic changes in developing retinal neurons result in regenerative
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<div xmlns:np="http://ncbi.gov/portal/XSLT/namespace" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance"></div><div class="portlet"><div class="portlet_head"><div class="portlet_title"><h3><span>Views</span></h3></div><a name="Shutter" sid="1" href="#" class="portlet_shutter" title="Show/hide content" remembercollapsed="true" pgsec_name="PDF_download" id="Shutter"></a></div><div class="portlet_content"><ul xmlns:np="http://ncbi.gov/portal/XSLT/namespace" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" class="simple-list"><li><a href="/books/NBK11505/?report=reader">PubReader</a></li><li><a href="/books/NBK11505/?report=printable">Print View</a></li><li><a data-jig="ncbidialog" href="#_ncbi_dlg_citbx_NBK11505" data-jigconfig="width:400,modal:true">Cite this Page</a><div id="_ncbi_dlg_citbx_NBK11505" style="display:none" title="Cite this Page"><div class="bk_tt">Gaillard F, Sauve Y. Fetal Tissue Allografts in the Central Visual System of Rodents. 2005 May 1 [Updated 2007 Jun 25]. In: Kolb H, Fernandez E, Jones B, et al., editors. Webvision: The Organization of the Retina and Visual System [Internet]. Salt Lake City (UT): University of Utah Health Sciences Center; 1995-. <span class="bk_cite_avail"></span></div></div></li><li><a href="/books/NBK11505/pdf/Bookshelf_NBK11505.pdf">PDF version of this page</a> (3.2M)</li><li><a href="/books/n/webvision/pdf/">PDF version of this title</a> (235M)</li></ul></div></div><div class="portlet"><div class="portlet_head"><div class="portlet_title"><h3><span>In this Page</span></h3></div><a name="Shutter" sid="1" href="#" class="portlet_shutter" title="Show/hide content" remembercollapsed="true" pgsec_name="page-toc" id="Shutter"></a></div><div class="portlet_content"><ul xmlns:np="http://ncbi.gov/portal/XSLT/namespace" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" class="simple-list"><li><a href="#ch34regeneration2.Introduction" ref="log$=inpage&amp;link_id=inpage">Introduction</a></li><li><a href="#ch34regeneration2.The_Visual_System_of" ref="log$=inpage&amp;link_id=inpage">The Visual System of Rodents: A Brief Overview</a></li><li><a href="#ch34regeneration2.Standard_Strategy_fo" ref="log$=inpage&amp;link_id=inpage">Standard Strategy for Intracerebral Transplantation: Graft Morphology</a></li><li><a href="#ch34regeneration2.Neurons_within_the_T" ref="log$=inpage&amp;link_id=inpage">Neurons within the Transplant Can Be Driven by Host Eye Visual Stimulation</a></li><li><a href="#ch34regeneration2.Do_Grafts_Receive_Ex" ref="log$=inpage&amp;link_id=inpage">Do Grafts Receive Extensive Afferents?</a></li><li><a href="#ch34regeneration2.Can_Grafts_Send_Affe" ref="log$=inpage&amp;link_id=inpage">Can Grafts Send Afferents to Host Targets?</a></li><li><a href="#ch34regeneration2.Restoration_of_Visua" ref="log$=inpage&amp;link_id=inpage">Restoration of Visual Behavior</a></li><li><a href="#ch34regeneration2.AFN1" ref="log$=inpage&amp;link_id=inpage">About the Authors</a></li><li><a href="#ch34regeneration2.References" ref="log$=inpage&amp;link_id=inpage">References</a></li></ul></div></div><div class="portlet"><div 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