Non-deprived Eye Research Articles

Synaptic Density in Geniculocortical Afferents Remains Constant after Monocular Deprivation in the Cat

Monocular eyelid closure in cats during a critical period in development produces both physiological plasticity, as indicated by a loss of responsiveness of primary visual cortical neurons to deprived eye stimulation, and morphological plasticity, as demonstrated by a decrease in the total length of individual geniculocortical arbors representing the deprived eye. Although the physiological plasticity appears maximal after 2 d of monocular deprivation (MD), the shrinkage of deprived-eye geniculocortical arbors is less than half-maximal at 4 d and is not maximal until 7 d of deprivation, at which time the deprived arbors are approximately half their previous size. To study this form of plasticity at the level of individual thalamocortical synapses rather than arbors, we developed a new double-label colocalization technique. First, geniculocortical afferent arbors serving either the deprived or nondeprived eye were labeled by injection of the anterograde tracer Phaseolus vulgaris leucoagglutinin into lamina A of the lateral geniculate nucleus. Then, using antibodies to synaptic vesicle proteins, we identified presynaptic terminals within the labeled arbors in layer IV of the primary visual cortex. Analysis of serial optical sections obtained using confocal microscopy allowed measurement of the numerical density of presynaptic sites and the relative amounts of synaptic vesicle protein in geniculocortical afferents after both 2 and 7 d of MD. We found that the density of synapses in geniculocortical axons was similar for deprived and nondeprived afferents, suggesting that this feature of the afferents is conserved even during periods in which synapse number is reduced by half in deprived-eye arbors. These results are not consistent with the hypothesis that a rapid loss of deprived-eye geniculocortical presynaptic sites is responsible for the prompt physiological effects of MD.

A role for choroidal lymphatics during recovery from form deprivation myopia?

The choroid of the chick swells markedly during recovery from experimentally induced myopia. It has been demonstrated previously that the lymphatic sinusoids of the choroid contribute most to the expansion. This raises important questions about the particular ultrastructural changes occurring in choroidal lymphatics as a means of understanding the role these vessels might play in emmetropization. Thirteen hatchling chicks were monocularly occluded for 2 weeks to induce myopia and then allowed normal visual experiences during recovery for periods of 0 to 72 h before sacrifice. Electron microscopic analysis detailed the temporal progression of vascular changes and provides qualitative evidence for edema in the extravascular space. Quantitative analysis showed that the frequency of open junctions between lymphatic endothelial cells (an indicator of passive fluid transfer) increased over the 3 days of recovery. Lymphatic fenestrations (an indicator of active fluid transfer) were rare in both nondeprived eyes and in form-deprived eyes at the time of occluder removal, but increased in density significantly over the first 24 h of recovery before returning to control levels by 72 h. The number of lymphatic endothelial caveolae did not change significantly during recovery, nor did the number of fenestrations along the walls of choriocapillaris vessels. The walls of the lymphatics of the chick choroid open to allow greater fluid transfer during re-emmetropization than normal; the lymphatics may play an important role in the maintenance of chorioretinal fluid balance and homeostasis.

The Critical Period for Ocular Dominance Plasticity in the Ferret’s Visual Cortex

Microelectrode recordings and optical imaging of intrinsic signals were used to define the critical period for susceptibility to monocular deprivation (MD) in the primary visual cortex of the ferret. Ferrets were monocularly deprived for 2, 7 or >14 d, beginning between postnatal day 19 (P19) and P110. The responses of visual cortical neurons to stimulation of the two eyes were used to gauge the onset, peak, and decline of the critical period. MDs ending before P32 produced little or no loss of response to the deprived eye. MDs of 7 d or more beginning around P42 produced the greatest effects. A rapid decline in cortical susceptibility to MD was observed after the seventh week of life, such that MDs beginning between P50 and P65 were approximately half as effective as those beginning on P42; MDs beginning after P100 did not reduce the response to the deprived eye below that to the nondeprived eye. At all ages, 2 d deprivations were 55-85% as effective as 7 d of MD. Maps of intrinsic optical responses from the deprived eye were weaker and less well tuned for orientation than those from the nondeprived eye, with the weakest maps seen in the hemisphere ipsilateral to the deprived eye. Analysis of the effects of 7 d and longer deprivations revealed a second period of plasticity in cortical responses in which MD induced an effect like that of strabismus. After P70, MD caused a marked loss of binocular responses with little or no overall loss of response to the deprived eye. The critical period measured here is compared to other features of development in ferret and cat.

TrkA activation in the rat visual cortex by antirat trkA IgG prevents the effect of monocular deprivation.

It has been recently shown that intraventricular injections of nerve growth factor (NGF) prevent the effects of monocular deprivation in the rat. We have tested the localization and the molecular nature of the NGF receptor(s) responsible for this effect by activating cortical trkA receptors in monocularly deprived rats by cortical infusion of a specific agonist of NGF on trkA, the bivalent antirat trkA IgG (RTA-IgG). TrkA protein was detected by immunoblot in the rat visual cortex during the critical period. Rats were monocularly deprived for 1 week (P21-28) and RTA-IgG or control rabbit IgG were delivered by osmotic minipumps. The effects of monocular deprivation on the ocular dominance of visual cortical neurons were assessed by extracellular single cell recordings. We found that the shift towards the ipsilateral, non-deprived eye was largely prevented by RTA-IgG. Infusion of RTA-IgG combined with antibody that blocks p75NTR (REX), slightly reduced RTA-IgG effectiveness in preventing monocular deprivation effects. These results suggest that NGF action in visual cortical plasticity is mediated by cortical TrkA receptors with p75NTR exerting a facilitatory role.

Critical period for the monocular deprivation effect in rats: assessment with sweep visually evoked potentials.

Rats and mice are the species most frequently used for cellular and biochemical studies of plasticity, but only a few studies have examined developmentally regulated visual plasticity in these species. Here we report a study of the critical period for monocular deprivation in Long-Evans rats in which visual pattern sweep evoked potentials (sweep VEP) was used. Successful recording of sweep VEPs depended on establishing a stable light plane of anesthesia. We found a mixture of halothane and NO2 to be suitable. During a single trial lasting 10 s, anesthetized rats (n = 28) viewed a sinusoidal contrast grating (spatial frequency of 0.13 cycles/deg) that reversed phase at 3 Hz. During the trial, the grating contrast increased logarithmically from 1 to 70%. Extracellular recording pipettes were placed bilaterally in layers II/III of the binocular regions of primary visual cortex. Stimulating the right and left eye on alternate trials, sweep VEP amplitudes were collected for 30 trials from each eye. In monocularly deprived animals, the right eyelid had been sutured for 5 days before recording. Age at suture varied from P19 to P86. In 12 of 13 rats sutured between P19 and P50, the crossed response from the deprived eye was smaller than the crossed response from the nondeprived eye. The same relation prevailed for the uncrossed responses in 11 of 13 animals. There was no significant monocular deprivation effect in animals sutured between P55 and P86 (n = 9). Dark rearing until approximately P90 followed by 5 days of eyelid suture resulted in a strong monocular deprivation effect in both crossed and uncrossed pathways (n = 3). There was little effect of dark rearing alone on the size the sweep VEPs (n = 3). The critical period reported here lasts at least 2 wk longer than reported for rats by Fagliolini et al. and for mice by Gordon and Stryker. Both previous studies used single unit recording rather than the sweep VEP method.

Morphology of Single Geniculocortical Afferents and Functional Recovery of the Visual Cortex after Reverse Monocular Deprivation in the Kitten

To investigate the possible anatomical basis for the functional recovery of visual cortical responses after reverse monocular deprivation, we have studied the morphology of single geniculocortical afferents to area 17. In kittens reverse-sutured for 10 d after an initial week of monocular deprivation, single-unit and intrinsic signal optical recordings confirmed that the effects of the initial deprivation were largely reversed. Responses through the originally nondeprived (OND) eye were drastically diminished, but remained much more selective for orientation than after an initial monocular deprivation (Crair et al., 1997). Responses through the originally deprived (OD) eye recovered completely. Geniculocortical afferent arbors in layer IV of area 17 were filled by iontophoresis of Phaseolus lectin into lamina A of the lateral geniculate nucleus (LGN) and were serially reconstructed. Arbors serving both the OD and the OND eye were analyzed. The plastic changes of both OD and OND arbors were evaluated by comparison with arbors reconstructed in normal animals and in animals studied after an equivalent initial period of deprivation (Antonini and Stryker, 1996). These analyses demonstrate that closure of the OND eye caused a substantial shrinkage of the arbors serving that eye. Moreover, reopening the OD eye induced regrowth only in some arbors, whereas others appeared to be largely unaffected and continued to have the characteristics of deprived arbors. Quantitatively, the initial and the second deprivation caused similar proportional changes in total arbor length and numbers of branches, whereas several other features were more severely affected by the initial deprivation.

Positional acuity in amblyopia: does a perceptual consequence of neural recruitment exist?

Animal models of amblyopia have shown that visual deprivation for even brief periods can result in dramatic changes in cortical architecture. Active neural recruitment mechanisms present the possibility that the non-deprived eye of amblyopes may show enhanced visual capacity. This idea was tested by measuring a form of positional acuity which we have termed alignment threshold. Three subject groups were examined, adults, visually normal children, and children with amblyopia in which the non-deprived eye was tested. Alignment thresholds in adults were significantly better (∼0.3 log unit) than the thresholds for visually normal children. No significant difference was found in thresholds between the visually normal children and the non-deprived eye of the amblyopic children. The results of this study suggest that subjects with unilateral amblyopia do not show enhanced visual alignment performance in their non-deprived eye.

Morphology of M-cell axon arbors in striate cortex of monkeys reared with monocular aphakia

Although the effects of visual deprivation on the development of ocular dominance columns have been well described in primates, nothing is known in primates about the impact of the deprivation on the axonal profiles that make up the ocular dominance columns. We now show that the effects of monocular deprivation on the morphology of geniculostriate axons involve not only shifts in terminal arbor sizes, much as would be expected from the ocular dominance data, but also changes in the proliferation of terminal arbor branches. In macaque monkeys reared from birth with unilateral lens removal (aphakia), terminal arbors of geniculostriate axons were bulk-filled with horseradish peroxidase (HRP) in brain-slice preparations and reconstructed from serial sections through striate cortex (area 17). Our focus was on the arbors that terminate in the upper tier of layer IV, the target of cells in the magnocellular (M) layers of the LGN. Of the 26 M-cell arbors reconstructed from three aphakic monkeys, eight were unique in having few very simple terminal arbor branches. These also tended to be smaller in total extent than the average M-cell axons reconstructed from 1 normal monkey. In contrast, eight arbors had very rich terminal branching patterns, and seven of these were larger than any of those from the normal monkey. We propose that the small, sparse axon arbors are related to the deprived eye, and the large, dense arbors are related to the non-deprived eye. These morphological changes reflect abnormalities in the growth patterns of geniculostriate inputs that undoubtedly have important persisting consequences for visual performance.

Optokinetic reflex in squirrel monkeys after long-term monocular deprivation.

Horizontal optokinetic nystagmus (OKN) as well as neuronal response properties in the nucleus of the optic tract and the dorsal terminal nucleus of the accessory optic system (NOT-DTN) were investigated in three monocularly deprived squirrel monkeys. In two monkeys occlusion of one eye was performed at birth (early) and in the third after 7 weeks (late). In adulthood, in early deprived monkeys monocular horizontal OKN tested through the non-deprived eye was symmetrical and in no way different from normal, i.e. stimulation in the temporonasal and nasotemporal direction elicited equal and robust responses. OKN through the early occluded eye, however, was grossly abnormal with low gain and great variability in the consistency of nasotemporal and temporonasal slow phase eye movements. When in the late deprived monkey the non-deprived eye was occluded a strong spontaneous nystagmus developed despite the deprived eye viewing a stationary pattern. The slow phases were directed from nasal to temporal for the deprived eye. When tested through the non-deprived eye all neuronal responses of the NOT-DTN were normal. The deprived eye's influence on NOT-DTN neurons was extremely weak. No neuron with a moderate or even dominant input from the deprived eye was found after early deprivation. In the late deprived case the deficit was not as severe but still the non-deprived eye was clearly dominating the responses in all neurons tested. Velocity tuning of neurons tested through the non-deprived eye was normal and qualitatively corresponded well to slow phase eye velocity in response to equivalent retinal slip during OKN. Through the early deprived eye, however, velocity tuning was extremely poor. It was somewhat better through the late deprived eye. We suggest that the dramatic deterioration in the optokinetic reflex found after long-term monocular deprivation for the amblyopic eye is probably caused by the almost complete loss of retinal and cortical input driven by that eye to the NOT-DTN. These results are discussed in relation to our previous results in cats and reports in the literature for humans with occlusion amblyopia.

Effect of sensory disuse on geniculate afferents to cat visual cortex.

In the kitten, as little as a week of monocular lid suture during early life causes a remarkable remodeling of the geniculocortical projections serving the deprived eye (Antonini & Stryker, 1993a, 1996). While the physiological effects of monocular deprivation have been shown to be due to competitive interactions between the projections serving the two eyes, it is not known whether these morphological changes are due to competitive interactions or to sensory disuse. We addressed this question by analyzing the morphology of geniculocortical arbors in kittens deprived of patterned vision by binocular lid suture for 1 week or 2 weeks ending at 6 weeks of age. Such deprivation would be expected to affect the afferents serving the two eyes equally, giving neither eye a competitive advantage. The arbors were anterogradely filled with Phaseolus lectin iontophoretically injected into lamina A of the lateral geniculate nucleus. The lectin was visualized immunohistochemically, and single geniculocortical arbors were serially reconstructed in three dimensions. Arbors reconstructed in binocularly deprived animals were compared with arbors serving the deprived and nondeprived eye in animals monocularly deprived by lid suture of one eye for a week and with arbors obtained in age-matched normal controls. Geniculocortical arbors in binocularly deprived animals did not suffer the drastic remodeling of the deprived arbors in monocularly deprived animals. Indeed, arbors in binocularly deprived animals were indistinguishable from arbors in normal kittens or nondeprived arbors in short-term monocularly deprived animals. These results support the notion that competitive mechanisms rather than sensory disuse are responsible for gross morphological remodeling of geniculocortical arbors.

Lack of lateral inhibitory interactions in visual cortex of monocularly deprived cats.

To gain new insight into the effects of monocular deprivation, we studied the visual cortex of adult cats deprived of vision in one eye. Local field potentials were recorded in response to contrast reversal of square-wave gratings modulated in time either by pseudorandom, m-sequences or periodically. We have found that: (1) stimulation of the retinotopic locus of the recording site elicits responses with abnormal waveforms and long latencies from the deprived eye; (2) stimulation of a remote, non-retinotopic locus elicits responses from the non-deprived eye but not from the deprived eye; (3) the monocularly deprived cortex lacks lateral inhibitory interactions which are characteristic of the normal cortex; and (4) steady-state responses showed little difference in spatial-frequency tuning and contrast sensitivity between the deprived and non-deprived eye, mostly conforming to earlier field-potential data in monocular deprivation. Functional lateral interactions appear to be greatly reduced in monocularly deprived cortex.

Relationship between the Ocular Dominance and Orientation Maps in Visual Cortex of Monocularly Deprived Cats

The significance of functional maps for cortical plasticity was investigated by imaging of intrinsic optical signals together with single-unit recording in kittens. After even a brief period of monocular deprivation during the height of the critical period, only isolated patches of visual cortex continued to respond strongly to the closed eye. These deprived-eye patches were located on the pinwheel center singularities of the orientation map and consisted of neurons that were poorly selective for stimulus orientation. Neurons in regions surrounding the deprived-eye patches responded only weakly to the deprived eye but were well tuned for the same stimulus orientation that optimally excited them when presented to the open, nondeprived eye. The coincidence of deprived-eye patches with pinwheel center singularities, and the selective loss of orientation tuning within the deprived-eye patches, indicate that the orientation and ocular dominance maps are functionally linked and provide compelling evidence that pinwheel center singularities are important for cortical plasticity.

Regional Scleral Changes in Form-deprivation Myopia in Chicks

Similar neurochemical events appear to be involved in the development of myopia in chicks and mammals. The rapid post-hatching development of the chick is ideal for studying experimental myopia. In this investigation, one eye of 2-day-old chicks was deprived of form vision for 2 weeks and then compared to the fellow, non-deprived eye by immunohistochemistry and light and electron microscopy.All deprived eyes showed a high refractive error and ocular enlargement. In deprived eyes, the posterior cartilaginous sclera was thicker and the fibrous sclera of the same section was thinner than the control. Scleral morphological changes were restricted to a central button 6–7 mm in diameter (the posterior pole) within the posterior hemisphere, further divided into posterotemporal and posteronasal parts. The most enlarged, posterior cartilaginous structure of deprived sclera could be divided into an inner and an outer zone. The inner zone had many unevenly-arranged chondrocytes, each having a well-developed granular endoplasmic reticulum and Golgi complex and a very irregular cell surface. Numerous S-phase cells and isogenous groups were detected in the outer zone. Hypertrophic chondrocytes were often observed in the innermost region of the outer zone and the outermost region of the inner zone. The boundary between the outer fibrous sclera and the cartilaginous sclera was irregular and obscured in myopic eyes. Spindle-shaped chondrocytes were seen to be in contact with each other. Thick collagen fibrils, usually seen only in the outer fibrous sclera, were present among the chondrocytes.Results of this morphological study suggest an increased proliferation of chondrocytes and active synthesis of extracellular matrix in visually deprived eyes. The elongation of the ocular axis that accompanies myopia is caused primarily by an active remodeling and differentiation in a restricted section of the posterior scleral cartilage. These facts indicate the posterior scleral cartilage may be more immature than cartilage in anterior and lateral segments.

Inhibition of nitric oxide synthase does not prevent ocular dominance plasticity in kitten visual cortex.

1. The neural messenger molecule nitric oxide (NO) has been shown to be involved in several forms of plasticity including hippocampal long-term potentiation. We examined the effects of chronic intracortical infusion of inhibitors of NO synthase (NOS) activity on the plasticity of visual cortical responses following monocular lid suture during the critical period. 2. Single unit recordings (618 cells) made in both the NOS inhibitor-treated (30 mM NG-methyl-L-arginine (L-NMMA), or 22 or 2 mM nitro-L-arginine (L-NOArg)) and saline-treated control hemispheres of barbiturate-anaesthetized, critical-period kittens (n = 8) revealed a profound shift in favour of the non-deprived eye. Shifts were of similar magnitude in hemispheres in which NOS was inhibited and in saline control hemispheres. 3. Subsequent analysis of NOS activity in the same cortical tissue in which recordings had been made showed a pronounced decrease in NOS activity in inhibitor-treated hemispheres. In the region in which all the single unit recordings were made (< 3 mm from the infusion cannula), 22 mM L-NOArg resulted in a reduction of NOS activity to 5.55 +/- 5.33% of control hemisphere NOS activity levels. L-NOArg (2 mM) and L-NMMA (30 mM) also produced clear, but smaller, inhibition of NOS activity. 4. These findings demonstrate that NOS activity is not essential for ocular dominance plasticity in visual cortex.

Plasticity of geniculocortical afferents following brief or prolonged monocular occlusion in the cat

During a critical period in early life, physiological studies reveal that either prolonged or brief periods of monocular occlusion induce similar plastic changes in the primary visual cortex (area 17) of the cat, leading to a nearly complete loss of visual responses from the deprived eye (Hubel and Wiesel [1970], J. Physiol. (London) 160: 106-154). However, the recovery of function is markedly different in the two conditions, being complete and thorough only after a brief period of monocular occlusion (Movshon [1976] J. Physiol. (London) 261: 125-174). In search for anatomical correlates that distinguish between these two experimental conditions, we compared the geniculocortical connectivity in normal kittens with that following brief (4 days and 6-7 days) or prolonged (> 5 weeks) periods of occlusion of vision in one eye. Transneuronal labeling of the geniculocortical pathway revealed changes in both cases, and single afferent arbors reconstructed in serial sections were similarly shrunken after short or long periods of deprivation. However, a significant expansion of the geniculocortical afferents serving the nondeprived eye was evident mainly after prolonged deprivation. These findings provide further evidence for rapid, activity-dependent remodeling of afferents during development.

Plasticity of geniculocortical afferents following brief or prolonged monocular occlusion in the cat

During a critical period in early life, physiological studies reveal that either prolonged or brief periods of monocular occlusion induce similar plastic changes in the primary visual cortex (area 17) of the cat, leading to a nearly complete loss of visual responses from the deprived eye (Hubel and Wiesel [1970], J. Physiol. (London) 160: 106–154). However, the recovery of function is markedly different in the two conditions, being complete and thorough only after a brief period of monocular occlusion (Movshon [1976] J. Physiol. (London) 261: 125–174). In search for anatomical correlates that distinguish between these two experimental conditions, we compared the geniculocortical connectivity in normal kittens with that following brief (4 days and 6–7 days) or prolonged (>5 weeks) periods of occlusion of vision in one eye. Transneuronal labeling of the geniculocortical pathway revealed changes in both cases, and single afferent arbors reconstructed in serial sections were similarly shrunken after short or long periods of deprivation. However, a significant expansion of the geniculocortical afferents serving the nondeprived eye was evident mainly after prolonged deprivation. These findings provide further evidence for rapid, activity-dependent remodeling of afferents during development. © 1996 Wiley-Liss, Inc.

Functional architecture of area 17 in normal and monocularly deprived marmosets (Callithrix jacchus).

The organization of the primary visual cortex (VI) of the common marmoset (Callithrix jacchus) was studied both physiologically and by means of transneuronal labelling of geniculocortical afferents. We addressed the question whether monocular deprivation (MD) could stabilize segregation into ocular dominance (OD) columns, which are not seen in normal adult marmosets but are present in juvenile animals (Spatz, 1979, 1989). Properties of neurons in normal marmosets closely resembled those of other New-World and Old-World monkeys and orderly tangential progressions of preferred orientation were observed. However, in contrast to species that display well-defined OD columns, neurons of layer 4 in V1 of normal adult marmosets received balanced inputs from the two eyes. Early MD (even though followed by prolonged binocular experience into adulthood) resulted in a reduction of cell size in laminae of the lateral geniculate nucleus with input from the deprived eye and a dramatic overall shift in ocular dominance towards the nondeprived eye in the cortex. However, isolated clusters of cells dominated by the deprived eye were found in both layers 4 and 6. Injection of lectin-conjugated horseradish peroxidase (WGA-HRP) into the deprived eye revealed elongated patches of terminal label, about 350 microns wide, in flat-mounted sections through layer 4. Afferent segregation was sharper and more regular in the region of V1 representing parafoveal visual space than in that representing the fovea. Our findings support the notion that all Old-World and New-World monkeys possess the capacity for segregation of geniculocortical afferents into OD columns.

Synaptic inputs to single neurons in the lateral geniculate nuclei of normal and monocularly deprived squirrel monkeys.

Neurons in the dorsal lateral geniculate nucleus (dLGN) of normal and monocularly lid-sutured squirrel monkeys were recorded electrophysiologically, and some were injected intracellularly with horseradish peroxidase (HRP) to examine and compare their synaptic inputs. Limited tests of the receptive field properties did not show any differences between the normal, nondeprived, or deprived neurons. Sixteen injected neurons were examined at the light microscopic level with most of these located in the P-laminae (n = 14). Ten of these were either from normal monkeys (n = 9) or received input from the nondeprived eye of a monocularly deprived monkey (n = 1). The remaining six neurons received input from the deprived eye. The dendritic trees of deprived neurons did not differ from those of normal or nondeprived neurons. Three normal and five deprived neurons from the P-laminae were examined at the electron microscopic level. Afferent distributions were not significantly different between normal and deprived neurons. Retinal, cortical, and gamma aminobutyric (GABA)ergic afferents accounted for nearly all inputs (avg., 42%, 23%, and 32%, respectively) and selectively contacted proximal, distal, or all parts of the dendrites. Overall, synaptic densities (synapses per length of dendrite) were high proximally and decreased with distance from the soma. However, the synaptic densities onto deprived neurons were higher at all distances compared to those onto normal neurons. Furthermore, HRP-filled deprived neurons received an average of 25 synapses onto their somata compared with only an average of 7 somal synapses on the HRP-filled normal neurons. Most of the increase in the number of synapses onto the deprived neurons was from GABAergic type profiles. This abnormality of the deprived neurons of the dLGN could be the underlying cause of their lesser responses compared with normal or nondeprived dLGN neurons. It could also be the initial stage that causes blindness in monocularly lid-sutured primates.

Transneuronal WGA-HRP: can it demonstrate development of ocular dominance patches and effects of monocular deprivation?

We have attempted to use intraocular injections of wheat germ agglutinin-horseradish peroxidase (WGA-HRP) to label ocular dominance patches in developing layer 4 of cat visual cortex. The cortices of animals killed at 49 days or later showed normal ocular dominance patches similar to those seen in [ 3H]proline material. Animals killed at 42 days showed some patches, but also showed unsegregated regions. Animals killed younger were difficult to stain and did not have patches. We also examined the ability of the WGA-HRP technique to demonstrate the effects of monocular deprivation (MD). MD for the first 3 months of life produced expansion of the afferents from the nondeprived eye and retraction of the patches from the deprived eye. One week of MD at about 5 weeks of age produced an expansion of the patches innervated by the nondeprived eye, but did not obviously affect the patches innervated by the deprived eye. We conclude that WGA-HRP is useful for examining the effects of long-term MD on ocular dominance patches but not for following the development of segregation. Its advantages over the [ 3H]proline technique are that it does not require a delay of many weeks before the sections can be examined and is much less expensive.

Depth perception in monocularly deprived cats following part-time reverse occlusion.

The behavioural effects of an early period of monocular deprivation can be extremely profound. However, it is possible to achieve a high degree of recovery, even to normal levels of visual acuity, by prompt imposition of certain regimes of part-time reverse occlusion where the initially non-deprived eye is occluded for only part of each day in order to allow a daily period of binocular visual exposure. In this paper we report on the depth perception of five monocularly deprived cats that had recovered normal visual acuity in both eyes following imposition of certain of the above occlusion regimes. Although three of the animals exhibited five- to sevenfold superiority of binocular over monocular depth thresholds, subsequent tests made on two of the animals revealed that they were unable to make stereoscopic discriminations with random-dot stereograms. Despite the recovery of normal visual acuity in both eyes, we conclude that these animals recover at best only local stereopsis.