Monocular Segment Research Articles

Comparative analysis of structural modifications induced by monocular retinal inactivation and monocular deprivation in the developing cat lateral geniculate nucleus.

During a critical period of postnatal life, monocular deprivation (MD) by eyelid closure reduces the size of neurons in layers of the dorsal lateral geniculate nucleus (dLGN) connected to the deprived eye and shifts cortical ocular dominance in favor of the non-deprived eye. Temporary inactivation of the non-deprived eye can promote superior recovery from the effects of long-term MD compared to conventional occlusion therapy. In the current study, we assessed the modification of neuron size in the dLGN as a means of measuring the impact of a brief period of monocular inactivation (MI) imposed at different postnatal ages. The biggest impact of MI was observed when it occurred at the peak of the critical period. Unlike the effect of MD, structural plasticity following MI was observed in both the binocular and monocular segments of the dLGN. With increasing age, the capacity for inactivation to alter postsynaptic cell size diminished but was still significant beyond the critical period. In comparison to MD, inactivation produced effects that were about double in magnitude and exhibited efficacy at older ages. Notwithstanding the large neural alterations precipitated by MI, its effects were remediated with a short period of binocular experience, and vision through the previously inactivated eye fully recovered. These results demonstrate that MI is a potent means of modifying the visual pathway and does so at ages when occlusion is ineffective. The efficacy and longevity of inactivation to elicit plasticity highlight its potential to ameliorate disorders of the visual system such as amblyopia.

Retinal lesions induce fast intrinsic cortical plasticity in adult mouse visual system.

Neuronal activity plays an important role in the development and structural-functional maintenance of the brain as well as in its life-long plastic response to changes in sensory stimulation. We characterized the impact of unilateral 15° laser lesions in the temporal lower visual field of the retina, on visually driven neuronal activity in the afferent visual pathway of adult mice using insitu hybridization for the activity reporter gene zif268. In the first days post-lesion, we detected a discrete zone of reduced zif268 expression in the contralateral hemisphere, spanning the border between the monocular segment of the primary visual cortex (V1) with extrastriate visual area V2M. We could not detect a clear lesion projection zone (LPZ) in areas lateral to V1 whereas medial to V2M, agranular and granular retrosplenial cortex showed decreased zif268 levels over their full extent. All affected areas displayed a return to normal zif268 levels, and this was faster in higher order visual areas than in V1. The lesion did, however, induce a permanent LPZ in the retinorecipient layers of the superior colliculus. We identified a retinotopy-based intrinsic capacity of adult mouse visual cortex to recover from restricted vision loss, with recovery speed reflecting the areal cortical magnification factor. Our observations predict incomplete visual field representations for areas lateral to V1 vs. lack of retinotopic organization for areas medial to V2M. The validation of this mouse model paves the way for future interrogations of cortical region- and cell-type-specific contributions to functional recovery, up to microcircuit level.

Homeostatic Plasticity in the Visual Thalamus by Monocular Deprivation

Monocular deprivation (MD) is a classic paradigm for experience-dependent cortical plasticity. One form is known as homeostatic plasticity, in which neurons innervated by the deprived eye show a remarkable capacity to compensate for degraded visual signals in an attempt to stabilize network activity. Although the evidence supporting homeostatic plasticity in visual cortex is extensive, it remains unclear whether neurons in subcortical visual structures respond to MD in a similar manner. Here we examined whether cells in the dorsal lateral geniculate nucleus (dLGN), the thalamic relay between the retina and visual cortex, show similar forms of experience-dependent homeostatic plasticity following MD. Two-week-old mice were monocularly deprived for a period of 5-7 d and miniature EPSCs (mEPSCs) were obtained from cells located in dLGN regions receiving input from the deprived or nondeprived eye. We found that MD promotes increases in the frequency and amplitude of mEPSCs and were restricted to the monocular segment contralateral to the deprived eye. These changes were accompanied by an increase in the probability of glutamate release at corticothalamic terminals that arise from the deprived visual cortex. Our findings indicate that homeostatic synaptic regulation from MD extends beyond cortical circuitry and shed light on how the brain modulates and integrates activity in the face of altered sensory experience.

Preceding Inhibition Silences Layer 6 Neurons in Auditory Cortex

A canonical feedforward circuit is proposed to underlie sensory cortical responses with balanced excitation and inhibition in layer 4 (L4). However, in another input layer, L6, sensory responses and the underlying synaptic circuits remain largely unclear. Here, cell-attached recordings in rat primary auditory cortex revealed that for the majority of L6 excitatory neurons, tonal stimuli did not drive spike responses, but suppressed spontaneous firings. Whole-cell recordings further revealed that the silencing resulted from tone-evoked strong inhibition arriving earlier than excitation. This pattern of inputs can be attributed to a parallel feedforward circuit with both excitatory and inhibitory inputs disynaptically relayed. In contrast, in the other neurons directly driven by thalamic input, stimuli evoked excitation preceding relatively weak inhibition, resulting in robust spike responses. Thus, the dichotomy of L6 response properties arises from two distinct patterns of excitatory-inhibitory interplay. The parallel circuit module generating preceding inhibition may provide a gating mechanism for conditional corticothalamic feedback.

Associative pairing involving monocular stimulation selectively mobilizes a subclass of GABAergic interneurons in the mouse visual cortex

Levels of gamma-aminobutyric acid (GABA) and its synthesizing enzyme in cerebral cortex are regulated by sensory experience. Previously we found that associative pairing of vibrissae stimulation and tail shock results in upregulation of GABAergic markers in the mouse barrel cortex. In order to ascertain whether GABAergic upregulation also accompanies associative pairing in other sensory modalities, we examined the mouse visual cortex after analogous training with visual stimulus. During pairing, visual stimulus (CS) was coupled with a tail shock (UCS). We examined the density of cells expressing glutamic acid decarboxylase (GAD) and parvalbumin (PV) in monocular and binocular segments of the primary visual cortex (V1). The auditory cortex was used as a control. After monocular training, the density of cells expressing GAD rose significantly in the monocular segment of V1 contralateral to the stimulated eye, compared with the opposite hemisphere. This effect was due to the association of CS and UCS, as no changes were found after visual stimulation alone or in the auditory cortex. No changes were noted in the density of PV(+) neurons, so the effect was attributed to GAD(+)/PV(-) neurons. Mobilization of a specific subclass of GABAergic cells, observed after associative pairing in the somatosensory and visual cortices, may reflect the necessity to restrict the activity of circuits involved in sensory association.

Misconvergence to the stimulus plane causes apparent displacement of the stimulus elements seen monocularly1

Abstract: When one binocularly views a group of vertical lines through a ring, the outermost line segments (one on each side) seen within the ring are seen monocularly while the segments of the same lines outside the ring are seen binocularly. The monocular segments appear to be displaced outward with respect to the center of the ring and with respect to the corresponding binocular segments outside the ring. Three experiments examined the extent and direction of this illusory displacement as a function of viewing distance, fixation disparity created by varying the angles of the two arms of a haploscope, and fixation disparity created by a stereoscope and different Nonius stimuli. The results of the experiments confirmed the hypothesis that the apparent displacement is due to misconvergence in accordance with Wells‐Hering's laws of visual direction.

Spontaneous Retinal Activity Mediates Development of Ocular Dominance Columns and Binocular Receptive Fields in V1

The mechanisms that give rise to ocular dominance columns (ODCs) during development are controversial. Early experiments indicated a key role for retinal activity in ODC formation. However, later studies showed that in those early experiments, the retinal activity perturbation was initiated after ODCs had already formed. Moreover, recent studies concluded that early eye removals do not impact ODC segregation. Here we blocked spontaneous retinal activity during the very early stages of ODC development. This permanently disrupted the anatomical organization of ODCs and led to a dramatic increase in receptive field size for binocular cells in primary visual cortex. Our data suggest that early spontaneous retinal activity conveys crucial information about whether thalamocortical axons represent one or the other eye and that this activity mediates binocular competition important for shaping receptive fields in primary visual cortex.

Spatial Analysis of Ocular Dominance Patterns in Monocularly Deprived Cats

Monocular deprivation during a critical period in postnatal development leads to a shift in functional and anatomical ocular dominance at the expense of the deprived eye. We analyzed the complete two-dimensional pattern of [(3)H]proline-labeled afferents in primary visual cortex (area 17) of cats monocularly deprived of vision at eye opening. Substantial shrinkage of deprived eye territory in favor of the normal eye extended into optic disc and monocular segment representations. However, small domains of deprived eye afferents were distributed evenly over the entire visual field representation. Interestingly, normal and deprived eye afferents overlapped extensively in the ipsilateral and in the peripheral contralateral visual field representation of the deprived eye, so that ipsi- and contralateral ocular dominance patterns are not at all complementary. We suggest that this could be the result of both an earlier maturation of crossed versus uncrossed visual pathways and of a maturational gradient within area 17 leading to a lower vulnerability of the central visual field representation to monocular deprivation. Quantitative analysis, using a triangulation algorithm which confirmed previously described larger spacing of adjacent ocular dominance columns in strabismic cats, revealed no difference in spacing of ocular dominance domains in area 17 between monocularly deprived and normals cats. In addition, column spacing was very similar in the same animal and in littermates, indicating that the genetic influence on columnar layout is stronger than previously assumed.

Amblyopia decreases activation of the corticogeniculate pathway and visual thalamic reticularis in attentive rats: a `focal attention' hypothesis

In rats which were rendered monocular amblyopic by lid suturing one eye during a critical period, the intensity of neuronal activation in parts of the monocular segments of the striate cortex (layers 4 and 6) and lateral geniculate nucleus, and in the visual segment of the thalamic reticular nucleus, was determined after exploration of a novel-complex environment. Quantitative analysis of the number of Fos-labelled neurons per unit area showed that, in comparison to the structures contralateral to the normal eye, in the side contralateral to the deprived amblyopic eye there is a gradient of diminished activation. The strongest activation asymmetry was observed in the visual reticular segment, while in layers 6 and 4 of the visual cortex the activation asymmetry was less strong and weakest, respectively. In the lateral geniculate there was no Fos-detectable activation asymmetry. Furthermore, there was a positive correlation between the time rats spent in exploration and the degree of activation asymmetry in the visual reticular segment. From these results it is concluded: (1) Activation of the visual segment of the thalamic reticular nucleus in the alert, attentive animal is predominantly under visual cortical control via the cortico-reticulo-geniculate pathway originating in layer 6, because this layer showed activation asymmetry while the other visual input to reticularis, the geniculate, did not show this asymmetry. (2) Activation of the visual reticularis is a function of attention to the environment because its activation asymmetry was correlated to the amount of exploratory attentional behaviour. (3) Diminished activity in the cortico-reticulo-geniculate pathway originating in layer 6, and of visual reticularis, caused by visual deprivation during the critical period should be considered as additional etiological factors of the resulting amblyopia. The functional significance of these results is explained by a `focal attention' hypothesis postulating that the observed activation of visual reticularis in exploring animals is necessarily a reflection of activation of the corticogeniculate pathway, because these axons innervate both the geniculate and the visual reticular segment. Mechanistically, a focus of animal's attention is transmitted in a top-down fashion from the extrastriate cortex, and from upper cortical layers, into striate cortex layer 6. In turn, activation of layer 6 cells corresponding to attentional foci generates a core of excitation in the geniculate by the direct glutamatergic corticogeniculate axons, and a surround inhibition by the disynaptic cortico–reticulo–geniculate (ultimately GABAergic) pathway. In the temporal domain, in light of recent results, activation of thalamic reticular nucleus visual segment will contribute to the induction of gamma oscillations in geniculocortical pathways and in their cortical targets. All together, these interactions result in increased effectiveness of thalamocortical transmission of features from the focalized visual scene. The postulated attention-dependent spatiotemporal influences on thalamocortical transmission would be a main function of the corticothalamic pathways in the awake, attentive animal.

Expression of DMAP-45R in the rat visual cortex is modulated by visual experience

Effects of visual experience upon expression of a developmentally regulated microtubule-associated protein (MAP) were studied in the visual cortex of monocularly deprived rats. The antibody Drosophila MAP-45 (DMAP-45) recognizes proteins in the developing ventral nerve cord of Drosophila and in rat brain. Monocular deprivation from day 12, before eye opening, to day 80 reduced the number of DMAP-45 immunoreactive layer V pyramidal cell apical dendrites in the monocular segment (Oc1M) of the visual cortex contralateral to the deprived eye. No significant visual deprivation effects were seen in the binocular segment (Oc1B). Immunoreactivity was restored to control levels in Oc1M of rats in which the monocular sutures were removed at day 75, subsequently allowing 5 days of exposure to light. These results indicate potential involvement of this MAP in experience-dependent structural plasticity.

Visual system of the fossorial mole‐lemmings, Ellobius talpinus and Ellobius lutescens

Ocular regression in subterranean species has been shown to be associated with a number of alterations in the retina and in retinal pathways. In order to examine the consequences of eye reduction, the visual system was studied in two species of the murine genus, Ellobius, a specialized fossorial rodent. The axial length of the eye is only 2.2 mm in E. lutescens and 2.9 mm in E. talpinus. The mean soma size of ganglion cells in Nissl-stained flatmounts is approximately 10 microns in E. lutescens and 12 microns in E. talpinus. The soma size distribution in both species appears unimodal and falls within a range of 6-17 microns in diameter. The topographic distribution of ganglion cells shows a weak centroperipheral gradient, and an area centralis cannot be distinguished. The total number of neurons in the ganglion cell layer in Nissl-stained flat mounts is 12,000 in E. lutescens and 28,500 in E. talpinus and, following injection of retrograde tracers in the superior colliculus, is, respectively, 3,600 and 20,000. Based on the axial length and maximum ganglion cell density, the calculated retinal magnification factor (20-26 microns/degree) and spatial resolution (0.4-0.9 cycles/degree) of these minute eyes are extremely reduced. Retinofugal projections, demonstrated by autoradiography and horseradish peroxidase histochemistry, are similar to those in other rodents. The superior colliculus is well developed and receives a predominantly contralateral projection. Ganglion cells projecting to the contralateral colliculus are distributed over the entire retina, while cells that project ipsilaterally are restricted to the ventrotemporal region. The dorsal lateral geniculate nucleus has clearly defined binocular and monocular segments, including a partial segregation of regions receiving ipsilateral or contralateral retinal innervation. In addition, a localized region of label is observed medial to the geniculate nucleus. The retina also sends a bilateral projection to the suprachiasmatic nucleus; the intergeniculate leaflet; the pretectum; and the medial, lateral, and dorsal terminal nuclei of the accessory optic system. Sparse retinal projections were also seen in the bed nucleus of the stria terminalis, the anterior thalamus, and the inferior colliculus. A substantial retinal projection is observed in the basal telencephalon, including the cortical amygdaloid region, the diagonal band of Broca, the olfactory tubercle, and the piriform cortex. The results suggest that the morphological constraints of reduced eye size are reflected in the retina by a generally homogeneous organization but that central visual projections are not substantially modified as in some more specialized, strictly subterranean rodents.

Numerical data on neocortical neurons in adult rat, with special reference to the GABA population

The disector method was used to estimate the numerical density of neurons (number per unit volume) and their actual number per column (number under a given area of pial surface), in the occipital (monocular segment of the primary visual area, Oc1M), the parietal (somatosensory barrelfield area, Par1) and the frontal cortex (primary motor area, Fr1) of adult rat. Values were first obtained for all neurons in each layer, and then for GABA neurons as identified with postembedding immunocytochemistry on semithin sections. The numerical density of neurons in the frontal cortex (34,000/mm 3) was significantly lower than in the two other neocortical areas (occipital: 52,000; parietal: 48,000/mm 3). The GABA population showed a similar difference and consequently represented an equivalent proportion of total (15%) in the three cortical areas. Across layers, there was an alternate distribution of low and high density of neurons from layers II–III to VI in the three cortical areas, with the highest density in layer IV of the two sensory areas. The laminar changes in density of the GABA neurons were not as pronounced as those of the overall population. Consequently, the layers with the highest overall neuronal densities tended to have a lower proportion of GABA neurons and vice versa. There were more neurons under 1 mm 2 of surface in the parietal (90,000) than the occipital or the frontal cortex (71,000), which was also true of the GABA neurons. The greater number of neurons per column in the parietal cortex was mostly imputable to layer IV, the main recipient of thalamic axons. Comparing these values from the rat with those previously obtained in cat and monkey, it seemed that the number of neurons per cortical column was the highest in the sensory area preferentially used by each species.

Effects of monocular deprivation on the visual fields of squirrel monkeys

Five squirrel monkeys were monocularly deprived at birth for 3 years. Visual field testing for the deprived eye revealed no responses to visual stimuli at any position, including the monocular segment. These results are similar to those obtained in macaque monkeys after long-term neonatal monocular deprivation and indicate that lack of patterned visual input to an eye during development in primates can produce functional blindness throughout the visual field. Because the monocular segment of the visual field was not spared, binocular competition cannot be the only mechanism underlying this loss. Instead, lack of patterned visual input probably causes improper neuronal connections during development in all segments of the visual cortex resulting in complete loss of form vision.

Morphological Changes in the Geniculocortical Pathway Associated with Monocular Deprivationa

To summarize (Fig. 10), the structural consequences of monocular deprivation include the following changes: the relay cells in the binocular segments of the deprived geniculate layers shrink and contain less of the possible neurotransmitter NAAG. These changes appear to be secondary to a loss of terminal synaptic arbor. Certainly, deprived geniculocortical cells project to smaller ocular dominance patches in layer IV of visual cortex, where they make fewer and abnormal synapses. As a result, they activate ocular activation columns that, in addition to being small, are faint and usually fail to extend into extragranular layers. This failure to extend to other layers probably results from a failure of the poorly activated deprived-eye cells in layer IV to compete successfully with neighboring experienced-eye cells in layer IV, resulting in a loss of connections from layer IV to other layers (Fig. 11). Thus, the primary effect of monocular deprivation is probably the disruption of the geniculocortical synapse, with the other changes, such as cell size, and possibly the change in neurotransmitter content, being secondary. The disrupted synapse would result in poorly driven cortical cells and faint ocular activation columns, which in turn would bias a secondary competition for access to cells in extragranular layers. There are certain general principles that unite the findings presented in this chapter with the others in this session. First, there are similarities in the types of morphological changes observed, for example, changes in the number and size of synaptic terminals, as well as mitochondrial changes. This implies that there are similar changes during development and adult plasticity and also similar changes in vertebrates and invertebrates. Second, it is not so much the amount of activity that determines these changes, but the pattern of activity. In my results, the relative imbalance in activity is important, but not the absolute amount (for example, the columns activated by the 8-hr eye of an AME 8/1 are different from those activated by the 8-hr eye of an AME 8/8). Similarly, the binocular segment, where there was an imbalance and competition could occur, was affected, whereas the monocular segment, where there was no imbalance and competition could not occur, was not. Finally, the recent results of Reiter and Stryker suggest that monocular deprivation produces changes only when the activity of the presynaptic cell and the postsynaptic cell are correlated.(ABSTRACT TRUNCATED AT 400 WORDS)

Retinal ganglion-cell densities and soma sizes are unaffected by long-term monocular deprivation in the cat

Three cats were raised with monocular deprivation for 5.2–7.2 years, and ganglion-cell densities and soma sizes were measured in their flat-mounted retinae. The retinae were Nissl-stained so that ganglion cells could be measured whether or not they maintained normal central projections. Measurements were made in the area centralis, peripheral binocular segment, and monocular segment of the retinae. There were no significant differences between the deprived and non-deprived retinae in the densities or soma-sizes of α cells or other (non-α) ganglion cells at any of these retinal locations. These results support the view that the most distal effects of monocular deprivation occur at the retino-geniculate contact, and they suggest that even after long-term monocular deprivation, effects in the lateral geniculate nucleus do not produce secondary, retrograde changes in the retina.

Retinofugal Projections in a Marsupial, <i>Tarsipes rostratus </i>(Honey Possum)

We examined the mature retinal projections of the honey possum, Tarsipes rostratus, an Australian, diprotodont marsupial, using uni-ocular injections of horseradish peroxidase and tetramethylbenzidine processing. The suprachiasmatic nucleus, medial, lateral and dorsal terminal nuclei of the accessory optic tract, pretectal nuclei and superior colliculus received bilateral retinal input. Contralateral input only was observed in the lateral posterior nucleus. The pattern of input to these regions was essentially similar to that seen in other marsupials. Cyto-architectural examination of the dorsal lateral geniculate nucleus (dLGN) indicated that 5 laminae were present in the alpha-segment, but the beta-segment appeared to lack lamination. Input to the dLGN was bilateral, overlapping considerably, and was organised in a laminar fashion with 7 and 3 terminal bands in the alpha- and beta-segments, respectively. The monocular segment accounted for 12% of the total volume of the dLGN. In the alpha-segment, 2 terminal bands each received exclusively contralateral or ipsilateral input and 3 bilateral input. In the beta-segment, 2 terminal bands received bilateral and 1 contralateral input. The volumes of the nucleus receiving contralateral and ipsilateral input were 77 and 54% of the total, respectively. A marked overlap of input from the two eyes is an unusual feature for a diprotodont marsupial and has previously been seen only in the feathertail glider. Our findings for the dLGN are of interest in the light of recent serological and taxonomic studies which suggest a close link between the feathertail glider and the honey possum.

Binocular competition affects the pattern and intensity of ocular activation columns in the visual cortex of cats

The effect of binocular competition on the development of ocular activation columns in areas 17 and 18 of cats was studied using the 14C-2-deoxyglucose (14C-2DG) technique to visualize the regions of cortex activated by one eye in cats reared with equal alternating monocular exposure (equal AME), unequal AME, or monocular deprivation (MD). The average size of the ocular activation columns of the eye stimulated during administration of 2DG was positively correlated with the competitive advantage during rearing. In order of increasing percentage of visual cortex activated, the eyes were (1) deprived eye of MD cats, (2) less experienced eye of unequal AME cats, (3) either eye of equal AME cats, (4) more experienced eye of unequal AME cats, and (5) experienced eye of MD cats. In area 17, the shape of the activation columns also was affected by the relative experience of the eye. The columns of the deprived eye of MD cats were widest in layer IV, where they were about the same width as those of the less experienced eye of the unequal AME cats; in other layers they were narrower, sometimes disappearing altogether. In contrast, the activation columns of the less experienced eye of the unequal AME cats were about the same width in all layers. These results suggest that when one eye is placed at a severe disadvantage and receives no patterned input, as in MD, both geniculocortical connections and intracortical connections may be disrupted, but when the disadvantage is less, as in unequal AME, only the geniculocortical connections are disrupted. Binocular competition also affected the intensity of activation within columns in area 17. We used video densitometry to determine ratios of the amount of label in cortical and thalamic structures. Both the ratio of label in area 17 to that in the lateral geniculate nucleus (LGN) and the ratio of label in the binocular segment of area 17 to that in the monocular segment were significantly less for the deprived eye of MD cats than for any other group. These results suggest that even within the smaller activation columns, deprived geniculocortical afferents are relatively ineffective at driving cortical cells. This finding is consistent with earlier reports that the synapses from the deprived pathway are both morphologically abnormal and reduced in number. The cortical labeling for the less experienced eye of the unequal AME cats and the experienced eye of the MD cats were also significantly less than that in equal AME cats.(ABSTRACT TRUNCATED AT 400 WORDS)

Effects of monocular occlusion and diffusion on visual system development in the cat

The effects of two forms of monocular deprivation (occlusion or diffusion) on visual system development were investigated. One group of cats monocularly deprived of all form stimulation but permitted diffuse light stimulation (diffusion, n = 4) during development showed a pattern of deficits similar to those reported for monocularly sutured cats. Most cells in the visual cortex were driven exclusively by the non-deprived eye and there were eye-specific deficits in X-cell acuity, proportion of Y-cells, and cell body size (binocular and monocular segment) in the lateral geniculate nucleus (LGN). A second group of cats monocularly deprived of all form and light stimulation (occlusion, n = 4) during development showed a less severe pattern of deficits. There was no acuity loss in LGN X-cells driven by the deprived eye, and cell body shrinkage was of smaller magnitude than in diffusion reared cats and was restricted to the binocular segment. Cortical deficits and LGN Y-cell loss were similar in the two groups. The results are consistent with the idea that monocular occlusion produces only deficits due to binocular competition while monocular diffusion reflects the combined effects of binocular competition and abnormal stimulation.

Effects of neonatal monocular and binocular enucleation on transient acetylcholinesterase activity in developing rat visual cortex

Geniculo-recipient layers of visual cortical area 17 in the laboratory rat display a transient pattern of acetylcholinesterase (AChE) activity during the second and third postnatal weeks of life. The appearance of the AChE histochemical reaction product and its distribution in thalamic recipient layers of cortical area 17 suggest that this transient AChE serves as a marker for the region of geniculocortical axon terminals. In the present study, infant rats were enucleated monocularly or binocularly on the day of birth. Animals were sacrificed at postnatal days 5–21. Frozen sections cut in either the transverse plane or parallel to the pial surface were processed for AChE histochemistry. Neonatal monocular enucleation resulted in a marked reduction of transient AChE activity in thalamic recipient layers of the medial part of area 17 contralateral to the enucleated orbit, i.e., the monocular segment of area 17. No loss of AChE was observed in area 17 ipsilateral to the enucleation. Pigmented and albino strains of rats did not differ significantly in the extent to which monocular enucleation reduced the transient AChE in contralateral visual cortex. Neonatal binocular enucleation resulted in an almost complete loss of AChE histochemical staining in thalamic recipient layers throughout cortical area 17, without loss of AChE in other cortical regions. These data support the hypothesis that transient AChE serves as a marker for the region of geniculocortical axon terminals, and also demonstrate that the transient expression of AChE in visual cortex depends upon normal innervation or activity of the geniculocortical neurons.

Changes in the size of cells in the monocular segment of the primate lateral geniculate nucleus during normal development and following visual deprivation

Cell areas have been measured in the monocular segment of the lateral geniculate nucleus in a series of 18 normal rhesus monkeys and in 27 following monocular or binocular lid closure or monocular enucleation. Cells in the parvocellular monocular segment shrank by 16% during the later period of normal development, between about 3 and 18 months of age, in contrast to cells in the binocular segment which did not. Monocular closure at birth caused hypertrophy of cells in the undeprived monocular segment whereas long-term closure started later caused shrinkage of both deprived and undeprived parvocellular cells additional to that occurring during normal development. In both these instances cells in the monocular segment related to the undeprived eye are undergoing changes indicating some form of binocular interaction even in the monocular segment, but these interactions are considerably weaker than in the binocular part of the nucleus. Enucleation caused marked transneuronal degeneration of cells in the contralateral monocular segment of both infant and adult monkeys.