A transient geniculo-extrastriate pathway in macaques? Implications for 'blindsight'

Both monkeys and cats receiving primary visual cortex lesions in infancy show better residual vision than animals sustaining similar damage in adulthood. In cats, the better recovery has been explained in part by stabilization of a transient pathway from the dorsal lateral geniculate nucleus (dLGN) to cortical visual area PMLS. To test the hypothesis that a similar transient pathway from the dLGN to dorsal extrastriate areas exists in primates and thus serves as a candidate for recruitment after early V1 damage, retrograde tracers were injected into areas MT, MST, and/or 7a of infant macaques. No evidence of a transient pathway from the dLGN to these areas was obtained, despite projections from the pulvinar and other extrastriate areas in all cases.     

Tritiated Uridine Uptake in the Retinal Ganglion Cell Layer of the Cat during Normal Development and after Visual Cortex Ablation

The short-term metabolic response of immature retinal ganglion cells to destruction of their target cells in the dorsal lateral geniculate nucleus (dLGN) was assessed in newborn cats. Retrograde degeneration of virtually all dLGN cells was induced by ablation of the 13 contiguous areas of visual cortex on the day of birth. The metabolic response of retinal ganglion cells to this loss of target cells in dLGN was determined by exposing the ganglion cell layer to tritiated uridine, a precursor of RNA. Control measurements were made from unoperated littermates. Following sectioning and processing of the retinae from both groups of kittens for autoradiography, silver grain densities overlying the cellular profiles in the ganglion cell layer were calculated. These calculations revealed levels of uridine incorporation at Postnatal Day 4 in both groups of kittens significantly higher than at either Postnatal Day 2 or 7, but no significant differences between the two groups on any day examined. These results show that the level of RNA synthesis in retinal ganglion cells increases temporarily during the first postnatal week and that this synthesis is unaffected by the death of target cells in the dLGN. The temporary increase may be related to the establishment of synaptic connections on retinal ganglion cells by their afferent bipolar and amacrine neurons in the inner nuclear layer.     

Topical organization of the extrageniculate visual system in the cat

Small electrolytic lesions were made in the superior colliculus of cats. The terminal areas of degenerated fibers from the lesions of the medial and lateral part of the superior colliculus were compared in the pretectum and in the pulvinar complex of the thalamus by utilizing the Nauta and Fink-Heimer technique. The medial part of the superior colliculus projects to the rostral and medial portion of the posterior pretectal nucleus, the nucleus of optic tract, and the dorsal half of the pulvinar complex. The lateral part of the superior colliculus projects to the suboptic and posterior pretectal nuclei and the nucleus of optic tract in the lateral pretectum, and to the ventral half of the pulvinar complex. These tectal projections to the pretectum and the pulvinar complex were compared with the terminal areas of the descending fibers from cortical areas 17 and 18. The results indicated that there is a retinotopic organization in the ascending projections from the superior colliculus in the cat.     

Prenatal and postnatal development of retinogeniculate and retinocollicular projections in the mouse

The development of retinal projections to the dorsal lateral geniculate nucleus (dLGN) and superior colliculus (SC) has been studied in fetal and neonatal mice of the pigmented C57BL/6 strain, using the anterograde transport of tritiated proline and horseradish peroxidase (HRP). Retinal efferents are present contralaterally just beyond the chiasm at E14. By E16 they have grown into both dLGN and SC. Ipsilateral fibers are limited to the proximal optic tract at E16; their growth into dLGN and SC is delayed until E18-birth. During the first 2 postnatal days, an early population of ipsilateral fibers invades the dLGN. Most of these fibers grow in or around the mediodorsal sector of the dLGN, i.e., the future binocular segment. Fibers are also present, but at lower densities, in the ventral half of the nucleus and thereafter become dispersed or are lost, without at any stage becoming dense. Some denser labeling is also present ipsilaterally in the outer rim of dLGN, just below the optic tract, and later disappears. On the third postnatal day, the ipsilateral fibers establish a deep and denser projection along the medial and dorsal borders of dLGN; this projection overlaps part of the crossed projection, which at this age extends to the whole nucleus. The segregation of each projection starts on the fourth postnatal day, when crossed fibers begin to disappear from the small region of uncrossed projection. This process goes on for another 4 days. During this period, the ipsilateral fibers withdraw from the deepest layer of dLGN, and their terminal density increases gradually; by the eighth postnatal day, both projections are already well separated. Dense crossed projections first appear near the surface of the SC at birth. Prior to this, retinal fibers course throughout neurons of the collicular plate and underneath the pia. The uncrossed fibers invade the SC between birth and P3. They are located preferentially in the anterior and medial aspect of the SC. Subsequently, there occurs a diminution in the laminar and tangential extent of these projections, simultaneously with an intensification of the ipsilateral input to several small, longitudinally oriented clusters located deep to the crossed projections.     

Investigation of cortical reorganization in area 17 and nine extrastriate visual areas through the detection of changes in immediate early gene expression as induced by retinal lesions

The effect of binocular central retinal lesions on the expression of the immediate early genes c-fos and zif268 in the dorsal lateral geniculate nucleus (dLGN) and the visual cortex of adult cats was investigated by in situ hybridization and immunocytochemistry. In the deafferented region of the dLGN, the c-fos mRNA level was decreased within 3 days. The dimensions of the geniculate region showing decreased amounts of c-fos mRNA matched the predictions based on the lesion size and the retinotopic maps of Sanderson ([1971] J. Comp. Neurol. 143:101-118). We did not detect zif268 mRNA in the dLGN. At the cortical level, both c-fos and zif268 mRNA expression decreased in the sensory-deprived region of area 17. In addition, the portions of areas 18, 19, 21a, 21b, and 7, as well as the posterior medial lateral suprasylvian area, the posterior lateral lateral suprasylvian area, the ventral lateral suprasylvian area, and the dorsal lateral suprasylvian area corresponding to the retinal lesions also displayed decreased c-fos and zif268 mRNA levels. Immunocytochemistry revealed similar changes for Zif268 and Fos protein. Three days post lesion, the dimensions of the lesion-affected cortical loci exceeded the predictions in relation to the size of the retinal lesions and the available retinotopic maps. Longer postlesion survival times clearly resulted in a time-dependent restoration of immediate early gene expression from the border to the center of the lesion-affected cortical portions. Our findings represent a new approach for investigating the capacity of adult sensory systems to undergo plastic changes following sensory deprivation and for defining the topographic nature of sensory subcortical and cortical structures.     

Immunocytochemistry and distribution of parabrachial terminals in the lateral geniculate nucleus of the cat: A comparison with corticogeniculate terminals

We used immunohistochemistry in cats to demonstrate the presence of brain nitric oxide synthase (BNOS) in cholinergic fibers within the A-laminae of the lateral geniculate nucleus. We used a double labeling procedure with electron microscopy and found that all terminals labeled for choline acetyltransferase (ChAT) in the geniculate A-laminae were double labeled for BNOS. Also, some interneuron dendrites, identified by labeling for γ-aminobutyric acid (GABA), contained BNOS, but relay cell dendrites did not. We then compared parabrachial and corticogeniculate terminals, identifying the former by BNOS/ChAT labeling and the latter by orthograde transport of biocytin injected into cortical area 17, 18, or 19. All corticogeniculate terminals and most BNOS- or ChAT-positive brainstem terminals displayed RSD morphology, whereas some brainstem terminals exhibited RLD morphology. However, parabrachial terminals were larger, on average, then corticogeniculate terminals. We also found that parabrachial terminals were located both inside and outside of glomeruli, and they always contacted relay cell dendrites proximally among retinal terminals (the retinal recipient zone). In contrast, the cortical terminals were limited to peripheral dendrites (the cortical recipient zone). Thus, little if any overlap exists in the distribution of parabrachial and corticogeniculate terminals on the dendrites of relay cells. J. Comp. Neurol. 377:535–549, 1997. © 1997 Wiley-Liss, Inc.     

Response of retinal terminals to loss of postsynaptic target neurons in the dorsal lateral geniculate nucleus of the adult cat.

We have used the neurotoxin kainic acid to produce rapid degeneration of neurons in the dorsal lateral geniculate nucleus (dLGN) of the adult cat. This degeneration mimics the rapid loss of geniculate neurons seen after visual cortex ablation in the neonate. Subsequent anterograde transport of horseradish peroxidase injected into the eye was used to reveal the projection patterns of retinal ganglion cell axons at different survival periods after the kainic acid injection. The density of retinal projections to the degenerated regions of the geniculate was reduced considerably at 4 and 6 months survival, but at 2 months was not significantly different from normal. The laminar pattern of projections to degenerated regions of the geniculate did not change in any animals studied, even when an adjacent lamina contained surviving cells. Electron microscopic examination of degenerated dLGN revealed intact retinal (RLP) and RSD terminals at all survival times, although the density of terminals appeared much reduced when compared to controls. Some RLP terminals exhibited the "dark reaction" of degeneration and these degenerating terminals were most numerous at 2 months survival. These findings demonstrate that, in response to degeneration of their usual target cells, mature retinal ganglion cells with withdraw their axon terminals from these regions of degeneration. We conclude that mature retinal ganglion cells continue to be dependent on target integrity for the maintenance of a normal axonal arborization.     

Differential display implicates cyclophilin A in adult cortical plasticity

Removal of retinal input from a restricted region of adult cat visual cortex leads to a substantial reorganization of the retinotopy within the sensory-deprived cortical zone. Little is known about the molecular mechanisms underlying this reorganization. We used differential mRNA display (DDRT-PCR) to compare gene expression patterns between normal control and reorganizing visual cortex (area 17-18), 3 days after induction of central retinal lesions. Systematic screening revealed a decrease in the mRNA encoding cyclophilin A in lesion-affected cortex. In situ hybridization and competitive PCR confirmed the decreased cyclophilin A mRNA levels in reorganizing cortex and extended this finding to longer postlesion survival times as well. Western blotting and immunocytochemistry extended these data to the protein level. In situ hybridization and immunocytochemistry further demonstrated that cyclophilin A mRNA and protein are present in neurons. To exclude the possibility that differences in neuronal activity per se can induce alterations in cyclophilin A mRNA and protein expression, we analyzed cyclophilin A expression in the dorsal lateral geniculate nucleus (dLGN) of retinally lesioned cats and in area 17 and the dLGN of isolated hemisphere cats. In these control experiments cyclophilin A mRNA and protein were distributed as in normal control subjects indicating that the decreased cyclophilin A levels, as observed in sensory-deprived area 17 of retinal lesion cats, are not merely a reflection of changes in neuronal activity. Instead our findings identify cyclophilin A, classically considered a housekeeping gene, as a gene with a brain plasticity-related expression in the central nervous system.     

Development of projections from auditory to visual areas in the cat

In newborn kittens, cortical auditory areas (including AI and AII) send transitory projections to ipsi- and contralateral visual areas 17 and 18. These projections originate mainly from neurons in supragranular layers but also from a few in infragranular layers (Innocenti and Clarke: Dev. Brain Res. 14:143-148, '84; Clarke and Innocenti: J. Comp. Neurol. 251:1-22, '86). The postnatal development of these projections was studied with injections of anterograde tracers (wheat germ agglutinin-horseradish peroxidase [WGA-HRP]) in AI and AII and of retrograde tracers (WGA-HRP, fast blue, diamidino yellow, rhodamine-labeled latex beads) in areas 17 and 18. It was found that the projections are nearly completely eliminated in development, this, by the end of the first postnatal month. Until then, most of the transitory axons seem to remain confined to the white matter and the depth of layer VI; a few enter it further but do not appear to form terminal arbors. As for other transitory cortical projections the disappearance of the transitory axons seems not to involve death of their neurons of origin. In kittens older than 1 month and in normal adult cats, retrograde tracer injections restricted to, or including, areas 17 and 18 label only a few neurons in areas AI and AII. Unlike the situation in the kitten, nearly all of these are restricted to layers V and VI. A similar distribution of neurons projecting from auditory to visual areas is found in adult cats bilaterally enucleated at birth, which suggests that the postnatal elimination of the auditory-to-visual projection is independent of visual experience and more generally of information coming from the retina.     

The absence of retinal input disrupts the development of cholinergic brainstem projections in the mouse dorsal lateral geniculate nucleus

Background

The dorsal lateral geniculate nucleus (dLGN) of the mouse has become a model system for understanding thalamic circuit assembly. While the development of retinal projections to dLGN has been a topic of extensive inquiry, how and when nonretinal projections innervate this nucleus remains largely unexplored. In this study, we examined the development of a major nonretinal projection to dLGN, the ascending input arising from cholinergic neurons of the brainstem. To visualize these projections, we used a transgenic mouse line that expresses red fluorescent protein exclusively in cholinergic neurons. To assess whether retinal input regulates the timing and pattern of cholinergic innervation of dLGN, we utilized the math5-null (math5^?/?) mouse, which lacks retinofugal projections due to a failure of retinal ganglion cell differentiation.

Results

Cholinergic brainstem innervation of dLGN began at the end of the first postnatal week, increased steadily with age, and reached an adult-like pattern by the end of the first postnatal month. The absence of retinal input led to a disruption in the trajectory, rate, and pattern of cholinergic innervation of dLGN. Anatomical tracing experiments reveal these disruptions were linked to cholinergic projections from parabigeminal nucleus, which normally traverse and reach dLGN through the optic tract.

Conclusions

The late postnatal arrival of cholinergic projections to dLGN and their regulation by retinal signaling provides additional support for the existence of a conserved developmental plan whereby retinal input regulates the timing and sequencing of nonretinal projections to dLGN.

     

Organization of immature intrahemispheric connections

In the adult cat injections of retrograde fluorescent tracers near the border between areas 17 and 18 and extending to the underlying white matter label neurons in restricted parts of nine other ipsilateral visual areas. A very similar, restricted distribution of retrograde labeling is found in newborn kittens when injections near the 17/18 border are confined to the cortical gray matter. When, however, the neonatal 17/18 border injection reaches the underlying white matter, more visual areas and numerous nonvisual areas become labeled, each of them over nearly its whole tangential extent. Labeled nonvisual areas include the primary and secondary auditory areas, the auditory areas of the posterior ectosylvian gyrus, areas 7 and 5, the cingulate gyrus, and the primary and secondary somatosensory areas. The widespread labeling in kittens was not due to larger or differently placed injections, since the distribution and extent of retrograde labeling in the ipsilateral lateral geniculate nucleus were similar at all ages. The transitory projections from the auditory and somatosensory areas are not reciprocated by a projection from areas 17 or 18. In kittens injected around the end of the first postnatal month the distribution of labeled association neurons is similar to that found in the adult; i.e., many of the juvenile projections have been eliminated. Only a few of the transitory axons to areas 17 and 18 enter the gray matter; the others remain confined to the white matter. Some of these axons were anterogradely labeled with rhodamine-B-iso-thiocyanate from the auditory cortex; they show bulbous endings, some of which are probably growth cones. Retrograde double-labeling experiments showed that, in the newborn, some neurons on the lateral sulcus have at least two long collaterals, one running rostrally, the other caudally; such branching is not observed in adults. In conclusion, areas 17/18 receive at birth from a large, continuous territory including areas, or parts of areas, which will later eliminate these projections. Most of the transitory projections do not appear to enter the cortex to any great extent. The major reshaping of association projections occurs before end of the first postnatal month. The development of association projections resembles that of callosal projections.     

Greater sparing of visually guided orienting behavior after early unilateral occipital lesions: insights from a comparison with the impact of bilateral lesions

We know that cats with bilateral lesions of occipital visual cortical areas 17, 18 and 19 sustained during the first postnatal week exhibit a modest level of sparing of the ability to re-orient head and eyes to new stimuli relative to cats that incurred equivalent lesions in adulthood. We now report that cats with equivalent unilateral lesions sustained during the first postnatal week (P1–4), or at the end of the first postnatal month (P27–30), orient to stimuli presented in the contralesional field as proficiently as to stimuli introduced into the ipsilesional field. Moreover, levels of proficiency are indistinguishable from those exhibited by intact cats. Thus, the sparing is greater following unilateral lesions than following bilateral lesions, and the level of sparing approaches completeness. The difference between the bilateral and unilateral lesion results suggests types of pathway reorganizations that may emerge as a result of unilateral occipital lesions. We postulate that the greater sparing is based on modifications in both excitatory and inhibitory circuitry linked to the intact hemisphere, and we provide a framework for future investigations that should be relevant to the comprehension of the repercussions of early unilateral and bilateral lesions sustained by monkeys and humans, which also show more robust residual vision following early relative to later damage of occipital cortex.     

Visual discrimination following infant and adult ablation of cortical areas 17, 18, and 19 in the cat.

Cats with ablations of visual cortical areas 17, 18, and 19 made in adulthood or infancy, and normal cats were trained on a light/dark and a horizontal/vertical discrimination. No differences between groups were observed in the light/dark discrimination. In the horizontal/vertical discrimination, adult operated cats showed severe deficits, but the performance of infant operated cats was similar to that of normal cats. Patterns of retrograde degeneration of the lateral geniculate nucleus differed for infant and adult operated cats: the lateral geniculate nucleus of infant operates, but not of adult operates, showed scattered intact surviving neurons which were not related to sparing of visual cortex. These nerons may be involved in pattern discrimination abilities in infant operated cats.     

Analysis of an experimental cortical network: II). Connections of visual areas 17 and 18 after neonatal injections of ibotenic acid.

Lesions of cortical areas 17 and 18 were produced in newborn kittens by local injections of the excitotoxin ibotenic acid. In the adult this results in a microcortex which consists of superficial layers I, II and III, in the absence of granular and infragranular layers. Horseradish peroxidase, alone or wheat germ agglutinin conjugated, was injected in the microcortex or in the contralateral, intact areas 17 and 18. The microcortex maintains several connections characteristic of normal areas 17 and 18 of the cat. It receives afferents from the dLGN, and several visual areas of the ipsilateral and contralateral hemisphere. However, it has lost its projections to dLGN, superior colliculus, and, at least in part, those to contralateral visual areas. Thus some parts of the microcortex receive from, but do not project into, the corpus callosum. In addition, the microcortex maintains afferents from ipsilateral and contralateral auditory areas AI and AII which are normally eliminated in development.     

Postnatal development of corticocortical efferents from area 17 in the cat's visual cortex

We are interested in the postnatal development of corticocortical connections in the cat's visual cortex. In this study, we injected the anterograde tracer 3H-proline into visual cortical area 17 of kittens, aged 4-70 d, and adult cats to visualize the distribution of terminals of the association projections to areas 18, 19, 21a, and the lateral suprasylvian visual cortex. The density of anterograde label was quantified using computerized image analysis. There was dense labeling at topographically appropriate locations in area 18 in animals of all ages. In 4- and 8-d-old kittens, other extrastriate areas (19, 21a and the lateral suprasylvian cortex) contained only sparse label, localized in a few solitary axons; these areas were densely labeled in animals aged 12 d or more. In kittens aged 4-20 d there was considerable, widespread label within fibers located in the white matter, and many of these axons lay underneath regions of extrastriate, and also striate, cortex that were almost certainly not destined to be persistently innervated by cells at the injection site. This pattern of extensive white matter label was not seen in animals older than 20 d. In each extrastriate region, from the earliest age at which we identified dense cortical innervation from area 17, the terminals were distributed in clusters. At first these patches were mainly in infragranular layers, but later, during the second and third postnatal weeks, they began to appear in more superficial laminae. By 70 d, an adult-like distribution of terminals was found in each extrastriate area: most fibers appeared to end in layers II and III in areas 18, 19, and 21a and centered on layer IV in the medial bank of the middle suprasylvian sulcus in adult cats. We suggest that the development of ipsilateral association projections from area 17 to extrastriate cortex is a 2-stage process. First, cells at a particular point in area 17 send immature fibers in a nonspecific fashion through white matter towards a very wide area of extrastriate cortex. Second, corticocortical axons penetrate extrastriate cortex mainly in patches at topographically appropriate regions and grow to their targets in a specific fashion.     

Organization of geniculocortical connections following prenatal interruption of binocular interactions

The organization of geniculostriate connections in normal cats was compared with that of adult animals that were uniocularly enucleated before birth. In normal animals microelectrophoretic deposits of horseradish peroxidase conjugated to wheat germ agglutinin (WGA-HRP) into the A-lamina of the dorsal lateral geniculate body (LGd) resulted in anterograde label in layers IV and VI and labeled cells in layer VI of areas 17 and 18. The labeling pattern within both of these cortical areas consisted of alternating patches separated by zones of equivalent size that were relatively free of label. In the normal animals no reaction product was evident in any other cortical area. In the prenatally enucleated cats, the LGd both contralateral and ipsilateral to the remaining eye is comprised of only two distinct cell layers. The dorsal layer appears to be a composite of the normal A/A1-laminae, while the ventral layer appears to correspond to the C-laminae. Deposits of WGA-HRP into the superficial aspect of the A/A1 layer yielded a dense continuous band of label within layers IV and VI of areas 17 and 18. Additionally, such deposits in the prenatally enucleated cats also revealed an anomalous reciprocal connection with area 19. Punctate deposits of WGA-HRP into cortical area 19 of the fetal enucleates resulted in the labeling of two distinct populations of cells within the A/A1 layer of the LGd. No cells were labeled within the A-laminae following such deposits into area 19 of normal animals. The geniculocortical connections of the prenatally enucleated cats, including that to area 19, were found to be retinotopically organized. These results indicate that in utero interruption of binocular interactions prevents the formation of ocular dominance domains within areas 17 and 18 of the cat's visual cortex. This could reflect the maintenance of exuberant geniculocortical projections present at the time of prenatal eye removal as originally suggested by Rakic (Science, 214 (1981) 928-931). The anomalous connection with area 19, on the other hand, could be due to the disruption of LGd cell migration resulting from the early eye removal.     

Generation and death of cells in the dorsal lateral geniculate nucleus and superior colliculus of the wallaby, Setonix brachyurus (quokka).

To study postnatal cell generation in primary visual centres of the quokka, tritiated thymidine was injected into pouch-young aged postnatal day (P)1-P85. Brains were examined at P100, just before eye-opening, when primary visual projections are essentially mature. Neurons in the dorsal lateral geniculate nucleus (dLGN) and superior colliculus (SC) were generated at P1-P10 and P1-P18 respectively. Peak numbers of labelled cells were seen at P3 and P5 in the dLGN and SC. Cell death was assessed in the dLGN and SC of young aged P10-P150. Low numbers of dying cells were seen in the dLGN throughout this period, with a small peak at P85. A more substantial peak of cell death was seen in the SC, also at P85. In the quokka, the time interval between the peaks of cell generation and of cell death in the dLGN and SC is 70-80 days, considerably longer than the interval of 40 days between birth and death of retinal cells.     

Abnormal ipsilateral visual field representation in areas 17 and 18 of hypopigmented cats

We compared the central projections of retinal ganglion cells in temporal retina and the cortical representation of visual fields in areas 17 and 18 in cats with various hypopigmentation phenotypes (albino, heterozygous albino, Siamese, and heterozygous Siamese). In all cats studied, we found that the extent of abnormal ipsilateral visual field representation varied widely, and more of the ipsilateral visual field was represented in area 18 than in area 17. The greatest degree of ipsilateral visual field representation was found in albino cats, followed by Siamese, heterozygous albino and heterozygote Siamese cats, respectively. Additionally, in the different groups there was wide variation in the numbers of contralaterally projecting alpha and beta ganglion cells in temporal retina. In all cases, however, contralaterally projecting alpha cells were found to extend further into temporal retina than beta cells. We found that in each cat studied, the maximum extent of the abnormal ipsilateral visual field representation in areas 18 and 17 corresponded to the location of the 50% decussation line (i. e., the point where 50% of the ganglion cells in temporal retina project to the contralateral hemisphere) for alpha and beta cells, respectively, for that cat. Our results suggest that the extent of the abnormal visual field representations in visual cortex of hypopigmented cats reflects the extent of contralaterally projecting retinal ganglion cells in temporal retina. © 1995 Wiley-Liss, Inc.     

Altered development of visual subcortical projections following neonatal thalamic ablation in the hamster

Previous research has demonstrated that precise patterns of axonal connectivity often develop during a series of stages characterized by pathfinding, target recognition, and address selection. This last stage involves the focusing of projections to a precisely defined region within the target. Because thalamic projections begin to innervate cortex before the latter stages are reached, these projections may be important in the establishment of adult-like patterns of cortical connectivity. To address this issue, we examined the mature corticopontine and corticospinal projections of visual cortex deprived of early thalamic input by visual thalamic ablation. Although ablations on the day of birth in hamsters did not disrupt the targeting of appropriate subcortical structures by visual cortical axons, they did alter the organization of projections within the basilar pons and spinal cord. The density and spread of visual corticopontine connections in lesioned animals was greatly increased relative to unlesioned animals, suggesting that thalamic afferents are required during address selection, when the topographic specificity of projections is established. To determine whether early visual thalamic ablation increases connectivity by stabilizing an exuberant developmental projection, we examined the normal development of visual corticopontine connections in hamsters ages postnatal days 1-17 (P1-P17). From the earliest ages, visual cortical axons innervate the pontine nucleus in regions specific to their adult projection zones and show progressive growth within these zones. At no time during development do projections exist that are equivalent to the projections found after thalamic ablation, suggesting that removal of thalamic input does not simply stabilize a developmental projection.     

The organization of the lateral geniculate nucleus and of the geniculocortical pathway that develops without retinal afferents

The fine structure and cortical connections of the dorsal lateral geniculate nucleus have been studied in postnatal (3.5-14-month-old) ferrets in which all retinal afferents had been removed prenatally at the time these fibers are first starting to invade the nucleus. The synaptic profiles in the mature nucleus show the cytological characteristics and arrangements that would remain if the retinal afferents were removed, with no significant compensatory ingrowth of foreign specific afferents. The nucleus is reduced in overall volume, but the geniculocortical and corticogeniculate interconnections show an essentially normal topography. Although in these experiments the geniculocortical projections can establish a normal topographic pattern in the absence of retinal afferents an accompanying paper shows that this topographic pattern can also be modified in the presence of abnormal retinogeniculate inputs. We conclude that two separate mechanisms contribute to the formation of retinal maps within the geniculocortical pathways and that different interactions between these two mechanisms produce the different patterns of abnormal geniculocortical pathways that have been described in pigment-deficient cats, mink and ferrets.