Non-deprived Eye Research Articles

Blockade of GluN2B-Containing NMDA Receptors Prevents Potentiation and Depression of Responses during Ocular Dominance Plasticity.

Monocular deprivation (MD) causes an initial decrease in synaptic responses to the deprived eye in juvenile mouse primary visual cortex (V1) through Hebbian long-term depression (LTD). This is followed by a homeostatic increase, which has been attributed either to synaptic scaling or to a slide threshold for Hebbian long-term potentiation (LTP) rather than scaling. We therefore asked in mice of all sexes whether the homeostatic increase during MD requires GluN2B-containing NMDA receptor activity, which is required to slide the plasticity threshold but not for synaptic scaling. Selective GluN2B blockade from 2-6 d after monocular lid suture prevented the homeostatic increase in miniature excitatory postsynaptic current (mEPSC) amplitude in monocular V1 of acute slices and prevented the increase in visually evoked responses in binocular V1 in vivo. The decrease in mEPSC amplitude and visually evoked responses during the first 2 d of MD also required GluN2B activity. Together, these results support the idea that GluN2B-containing NMDA receptors first play a role in LTD immediately following eye closure and then promote homeostasis during prolonged MD by sliding the plasticity threshold in favor of LTP.

Collective plasticity of binocular interactions in the adult visual system

Binocular visual plasticity can be initiated via either bottom-up or top-down mechanisms, but it is unknown if these two forms of adult plasticity can be independently combined. In seven participants with normal binocular vision, sensory eye dominance was assessed using a binocular rivalry task, before and after a period of monocular deprivation and with and without selective attention directed towards one eye. On each trial, participants reported the dominant monocular target and the inter-ocular contrast difference between the stimuli was systematically altered to obtain estimates of ocular dominance. We found that both monocular light- and pattern-deprivation shifted dominance in favour of the deprived eye. However, this shift was completely counteracted if the non-deprived eye’s stimulus was selectively attended. These results reveal that shifts in ocular dominance, driven by bottom-up and top-down selection, appear to act independently to regulate the relative contrast gain between the two eyes.

The Suppressive Basis of Ocular Dominance Changes Induced by Short-Term Monocular Deprivation in Normal and Amblyopic Adults.

We aimed to study the effect of short-term monocular deprivation on the suppressive interocular interactions in normals and amblyopes by using a dichoptic masking paradigm. Nine adults with anisometropic or mixed amblyopia and 10 control adults participated in our study. The contrast sensitivity in discriminating a target Gabor dichoptically masked was measured before and after 2 hours of monocular deprivation. The mask consisted of bandpass-filtered noise. Both the target and the mask were horizontally oriented at the spatial frequency of 1.31 cpd. Deprivation was achieved using an opaque patch on the amblyopic eye of amblyopes and the dominant eye of controls. Results were similar in both controls and amblyopes. After 2 hours of monocular deprivation, the previously patched eye showed a significant increase in contrast sensitivity under dichoptic masking, which also suggested reduced suppressive effect from the nonpatched eye. Meanwhile, the contrast sensitivity of the nonpatched eye remained almost unchanged under dichoptic masking. We demonstrate that the ocular dominance changes induced by short-term monocular deprivation-namely, the strengthening of the deprived eye's contribution-are associated with the unilateral and asymmetric changes in suppressive interaction. The suppression from the nondeprived eye is reduced after short-term monocular deprivation. This provides a better understanding of how inverse patching (patching of the amblyopic eye) could, by reducing the suppressive drive from the normally sighted (nondeprived) eye, form the basis of a new treatment for the binocular deficit in amblyopia.

Experience dependent plasticity of higher visual cortical areas in the mouse.

Experience dependent plasticity in the visual cortex is a key paradigm for the study of mechanisms underpinning learning and memory. Despite this, studies involving manipulating visual experience have largely been limited to the primary visual cortex, V1, across various species. Here we investigated the effects of monocular deprivation (MD) on the ocular dominance (OD) and orientation selectivity of neurons in four visual cortical areas in the mouse: the binocular zone of V1 (V1b), the putative "ventral stream" area LM and the putative "dorsal stream" areas AL and PM. We employed two-photon calcium imaging to record neuronal responses in young adult mice before MD, immediately after MD, and following binocular recovery. OD shifts following MD were greatest in LM and smallest in AL and PM; in LM and AL, these shifts were mediated primarily through a reduction of deprived-eye responses, in V1b and LM through an increase in response through the non-deprived eye. The OD index recovered to pre-MD levels within 2weeks in V1 only. MD caused a reduction in orientation selectivity of deprived-eye responses in V1b and LM only. Our results suggest that changes in OD in higher visual areas are not uniformly inherited from V1.

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.

Crossmodal plasticity following short-term monocular deprivation

A brief period of monocular deprivation (MD) induces short-term plasticity of the adult visual system. Whether MD elicits neural changes beyond visual processing is yet unclear. Here, we assessed the specific impact of MD on neural correlates of multisensory processes. Neural oscillations associated with visual and audio-visual processing were measured for both the deprived and the non-deprived eye. Results revealed that MD changed neural activities associated with visual and multisensory processes in an eye-specific manner. Selectively for the deprived eye, alpha synchronization was reduced within the first 150 ms of visual processing. Conversely, gamma activity was enhanced in response to audio-visual events only for the non-deprived eye within 100–300 ms after stimulus onset. The analysis of gamma responses to unisensory auditory events revealed that MD elicited a crossmodal upweight for the non-deprived eye. Distributed source modeling suggested that the right parietal cortex played a major role in neural effects induced by MD. Finally, visual and audio-visual processing alterations emerged for the induced component of the neural oscillations, indicating a prominent role of feedback connectivity. Results reveal the causal impact of MD on both unisensory (visual and auditory) and multisensory (audio-visual) processes and, their frequency-specific profiles. These findings support a model in which MD increases excitability to visual events for the deprived eye and audio-visual and auditory input for the non-deprived eye.

Primate monocular vision is intrinsically unstable: a side-effect of binocular homeostasis

Short-term deprivation of one eye of 1-2 hours in human adults results in reciprocal changes in the interocular balance that last 30-90 minutes, assumed to be the consequence of a change in the contrast gain within the binocular circuitry. What is not known is how these changes emerge and with what dynamic. One possibility is that they are initiated once the patch is removed. The alternative is that they result from a dynamic build-up from the moment the patch is applied. In this study, we measure the monocular dynamics of the non-deprived eye activation during the deprivation of the other eye in humans, using psychophysics, and in awake non-human primates, using functional ultrasound imaging (fUS) of the primary visual cortex (V1). In humans, we show that the contrast threshold increases overtime during the deprivation of the other eye. This observation indicates that the patching effect slowly builds up over the deprivation period at a binocular site. In the awake macaque, we show that during monocular deprivation the cerebral blood volume (CBV) increases in the non-deprived eye ocular-dominance bands, but not the deprived eye bands with similar dynamics as observed in human psychophysics. We show that human behavioral results can be predicted by a simple interocular normalization model that uses non-human primate CBV dynamics as a descriptor of the normalization pool activity. In conclusion, our results highlight a hitherto unknown feature of primate vision: monocular vision per se is intrinsically unstable.

Neuromodulation in the developing visual cortex after long-term monocular deprivation.

Neural dynamics are altered in the primary visual cortex (V1) during critical period monocular deprivation (MD). Synchronization of neural oscillations is pertinent to physiological functioning of the brain. Previous studies have reported chronic disruption of V1 functional properties such as ocular dominance, spatial acuity, and binocular matching after long-term monocular deprivation (LTMD). However, the possible neuromodulation and neural synchrony has been less explored. Here, we investigated the difference between juvenile and adult experience-dependent plasticity in mice from intracellular calcium signals with fluorescent indicators. We also studied alterations in local field potentials power bands and phase-amplitude coupling (PAC) of specific brain oscillations. Our results showed that LTMD in juveniles causes higher neuromodulatory changes as seen by high-intensity fluorescent signals from the non-deprived eye (NDE). Meanwhile, adult mice showed a greater response from the deprived eye (DE). LTMD in juvenile mice triggered alterations in the power of delta, theta, and gamma oscillations, followed by enhancement of delta-gamma PAC in the NDE. However, LTMD in adult mice caused alterations in the power of delta oscillations and enhancement of delta-gamma PAC in the DE. These markers are intrinsic to cortical neuronal processing during LTMD and apply to a wide range of nested oscillatory markers.

Short-term plasticity in the human visual thalamus.

While there is evidence that the visual cortex retains a potential for plasticity in adulthood, less is known about the subcortical stages of visual processing. Here, we asked whether short-term ocular dominance plasticity affects the human visual thalamus. We addressed this question in normally sighted adult humans, using ultra-high field (7T) magnetic resonance imaging combined with the paradigm of short-term monocular deprivation. With this approach, we previously demonstrated transient shifts of perceptual eye dominance and ocular dominance in visual cortex (Binda et al., 2018). Here, we report evidence for short-term plasticity in the ventral division of the pulvinar (vPulv), where the deprived eye representation was enhanced over the nondeprived eye. This vPulv plasticity was similar as previously seen in visual cortex and it was correlated with the ocular dominance shift measured behaviorally. In contrast, there was no effect of monocular deprivation in two adjacent thalamic regions: dorsal pulvinar and Lateral Geniculate Nucleus. We conclude that the visual thalamus retains potential for short-term plasticity in adulthood; the plasticity effect differs across thalamic subregions, possibly reflecting differences in their corticofugal connectivity.

Assessing the impact of monocular deprivation on visual evoked potentials, behavior, and visual plasticity in juvenile mice.

BackgroundThe physiological mechanisms which underlie amblyopia are predicted using animal models which assess the impact of amblyogenic factors on visual function. This study used monocular-deprived mice as an amblyopic model to assess visual function by flash visual evoked potentials (fVEP), behavioral assessment, and visual plasticity.MethodsA total of 294 C57BL/6J mice (both genders) were used in this study. The mice were divided into the normal control (NC) group and monocular deprivation (MD) group. After mice were anesthetized with pentobarbital, fVEP was recorded. Long-term potentiation (LTP) was recorded from primary visual cortex slices. Behavioral assessment of visual function was performed using a visual water trapezoidal-shaped pool with a release chute, a hidden platform, and a middle divider.ResultsAll fVEP results showed that N1 waves and P2 waves were repeatable and N1–P2 amplitude was the most stable indicator. The amplitude of N1–P2 of MD eyes was significantly lower than that of non-deprived eyes or NC eyes. LTP failed to be induced in the visual cortex V1 area corresponding to deprived eyes in the MD group but could be induced successfully in the visual cortex V1 area corresponding to non-deprived eyes in the MD group. Behavioral vision testing also showed a longer time to reach the platform in MD mice compared to NC mice. The correlation coefficient suggested that LTP is the better indicator for visual impairment.ConclusionsThe fVEP can be utilized as an index of amblyopic changes in mice, which correlates well with behavioral results.

Correction of amblyopia in cats and mice after the critical period.

Monocular deprivation early in development causes amblyopia, a severe visual impairment. Prognosis is poor if therapy is initiated after an early critical period. However, clinical observations have shown that recovery from amblyopia can occur later in life when the non-deprived (fellow) eye is removed. The traditional interpretation of this finding is that vision is improved simply by the elimination of interocular suppression in primary visual cortex, revealing responses to previously subthreshold input. However, an alternative explanation is that silencing activity in the fellow eye establishes conditions in visual cortex that enable the weak connections from the amblyopic eye to gain strength, in which case the recovery would persist even if vision is restored in the fellow eye. Consistent with this idea, we show here in cats and mice that temporary inactivation of the fellow eye is sufficient to promote a full and enduring recovery from amblyopia at ages when conventional treatments fail. Thus, connections serving the amblyopic eye are capable of substantial plasticity beyond the critical period, and this potential is unleashed by reversibly silencing the fellow eye.

Ocular dominance columns in V1 are more susceptible than associated callosal patches to imbalance of eye input during precritical and critical periods.

In Long Evans rats, ocular dominance columns (ODCs) in V1 overlap with patches of callosal connections. Using anatomical tracers, we found that ODCs and callosal patches are present at postnatal day 10 (P10), several days before eye opening, and about 10 days before the activation of the critical period for ocular dominance plasticity (~P20). In rats monocularly enucleated at P10 and perfused ~P20, ODCs ipsilateral to the remaining eye desegregated, indicating that rat ODCs are highly susceptible to monocular enucleation during a precritical period. Monocular enucleation during the critical period exerted significant, although smaller, effects. Monocular eye lid suture during the critical period led to a significant expansion of the ipsilateral projection from the nondeprived eye, whereas the contralateral projection invaded into, and intermixed with, ipsilateral ODCs innervated by the deprived eye. We propose that this intermixing allows callosal connections to contribute to the effects of monocular deprivation assessed in the hemisphere ipsilateral to the nondeprived eye. The ipsilateral and contralateral projections from the deprived eye did not undergo significant shrinkage. In contrast, we found that callosal patches are less susceptible to imbalance of eye input. In rats monocularly enucleated during either the precritical or critical periods, callosal patches were maintained in the hemisphere ipsilateral to the remaining eye, but desegregated in the hemisphere ipsilateral to the enucleated orbit. Callosal patches were maintained in rats binocularly enucleated at P10 or later. Similarly, monocular deprivation during the critical period had no significant effect on callosal patches in either hemisphere.

The ups and downs of sensory eye balance: Monocular deprivation has a biphasic effect on interocular dominance

Classic studies of ocular dominance plasticity in early development showed that monocular deprivation suppresses the neural representation and visual function of the deprived eye. However, recent studies have shown that a short period of monocular deprivation (<3 h) in normal adult humans, shifts sensory eye dominance in favor of the deprived eye. How can these opposing effects be reconciled? Here we argue that there are two systems acting in opposition at different time scales. A fast acting, stabilizing, homeostatic system that rapidly decreases gain in the non-deprived eye or increases gain in the deprived eye, and a relatively sluggish system that shifts balance toward the non-deprived eye, in an effort to reduce input of little utility to active vision. If true, then continuous deprivation should produce a biphasic effect on interocular balance, first shifting balance away from the non-deprived eye, then towards it. Here we investigated the time course of the deprivation effect by monocularly depriving typical adults for 10 h and conducting tests of sensory eye balance at six intervening time points. Consistent with previous short-term deprivation work, we found shifts in sensory eye dominance away from the non-deprived eye up until approximately 5 h. We then observed a turning point, with balance shifting back towards the non-deprived eye, -, a biphasic effect. We argue that this turning point marks where the rapid homeostatic response saturates and is overtaken by the slower system responsible for suppressing monocular input of limited utility.

Brief period of monocular deprivation drives changes in audiovisual temporal perception

The human brain retains a striking degree of plasticity into adulthood. Recent studies have demonstrated that a short period of altered visual experience (via monocular deprivation) can change the dynamics of binocular rivalry in favor of the deprived eye, a compensatory action thought to be mediated by an upregulation of cortical gain control mechanisms. Here, we sought to better understand the impact of monocular deprivation on multisensory abilities, specifically examining audiovisual temporal perception. Using an audiovisual simultaneity judgment task, we discovered that 90 minutes of monocular deprivation produced opposing effects on the temporal binding window depending on the eye used in the task. Thus, in those who performed the task with their deprived eye there was a narrowing of the temporal binding window, whereas in those performing the task with their nondeprived eye there was a widening of the temporal binding window. The effect was short lived, being observed only in the first 10 minutes of postdeprivation testing. These findings indicate that changes in visual experience in the adult can rapidly impact multisensory perceptual processes, a finding that has important clinical implications for those patients with adult-onset visual deprivation and for therapies founded on monocular deprivation.

Silent Synapse-Based Mechanisms of Critical Period Plasticity.

Critical periods are postnatal, restricted time windows of heightened plasticity in cortical neural networks, during which experience refines principal neuron wiring configurations. Here, we propose a model with two distinct types of synapses, innate synapses that establish rudimentary networks with innate function, and gestalt synapses that govern the experience-dependent refinement process. Nascent gestalt synapses are constantly formed as AMPA receptor-silent synapses which are the substrates for critical period plasticity. Experience drives the unsilencing and stabilization of gestalt synapses, as well as synapse pruning. This maturation process changes synapse patterning and consequently the functional architecture of cortical excitatory networks. Ocular dominance plasticity (ODP) in the primary visual cortex (V1) is an established experimental model for cortical plasticity. While converging evidence indicates that the start of the critical period for ODP is marked by the maturation of local inhibitory circuits, recent results support our model that critical periods end through the progressive maturation of gestalt synapses. The cooperative yet opposing function of two postsynaptic signaling scaffolds of excitatory synapses, PSD-93 and PSD-95, governs the maturation of gestalt synapses. Without those proteins, networks do not progress far beyond their innate functionality, resulting in rather impaired perception. While cortical networks remain malleable throughout life, the cellular mechanisms and the scope of critical period and adult plasticity differ. Critical period ODP is initiated with the depression of deprived eye responses in V1, whereas adult ODP is characterized by an initial increase in non-deprived eye responses. Our model proposes the gestalt synapse-based mechanism for critical period ODP, and also predicts a different mechanism for adult ODP based on the sparsity of nascent gestalt synapses at that age. Under our model, early life experience shapes the boundaries (the gestalt) for network function, both for its optimal performance as well as for its pathological state. Thus, reintroducing nascent gestalt synapses as plasticity substrates into adults may improve the network gestalt to facilitate functional recovery.

Natural-scene-based Steady-state Visual Evoked Potentials Reveal Effects of Short-term Monocular Deprivation

Ocular dominance plasticity beyond the critical period has been demonstrated in adult humans in recent investigations of short-term monocular deprivation (MD). To our knowledge, all previous research adopted non-natural synthetic stimuli in testing perceptual ocular dominance before and after the MD. However, it is recognized that complex natural stimuli may engage cortical mechanisms substantially different from simple synthetic stimuli. Therefore, it remains largely unknown whether reshaping of ocular dominance following MD could be observed during perception of natural scene stimuli without conspicuous interocular competition. Here we used the steady-state visual evoked potential (SSVEP) technique to measure the ocular-specific neural effects of MD with natural scene stimuli where the two eyes’ images were tagged with different frequencies. Two hours of MD boosted the neural gain for the deprived eye. During the course of MD, the SSVEP amplitude ratio for the deprived eye compared to the non-deprived eye increased significantly over time, indicating a progressive increase of neural gain for the deprived eye. These findings demonstrate that the effects of short-term MD can manifest when viewing natural scenes, providing a natural case in support of the homeostatic compensation theory of MD. Our work also indicates that the technique of natural-scene-based SSVEP could be particularly useful for future work exploring the neural dynamics during adaptation to natural stimuli.

17\u03b1 Estradiol promotes plasticity of spared inputs in the adult amblyopic visual cortex

The promotion of structural and functional plasticity by estrogens is a promising approach to enhance central nervous system function in the aged. However, how the sensitivity to estrogens is regulated across brain regions, age and experience is poorly understood. To ask if estradiol treatment impacts structural and functional plasticity in sensory cortices, we examined the acute effect of 17α-Estradiol in adult Long Evans rats following chronic monocular deprivation, a manipulation that reduces the strength and selectivity of deprived eye vision. Chronic monocular deprivation decreased thalamic input from the deprived eye to the binocular visual cortex and accelerated short-term depression of the deprived eye pathway, but did not change the density of excitatory synapses in primary visual cortex. Importantly, we found that the classical estrogen receptors ERα and ERβ were robustly expressed in the adult visual cortex, and that a single dose of 17α-Estradiol reduced the expression of the calcium-binding protein parvalbumin, decreased the integrity of the extracellular matrix and increased the size of excitatory postsynaptic densities. Furthermore, 17α-Estradiol enhanced experience-dependent plasticity in the amblyopic visual cortex, by promoting response potentiation of the pathway served by the non-deprived eye. The promotion of plasticity at synapses serving the non-deprived eye may reflect selectivity for synapses with an initially low probability of neurotransmitter release, and may inform strategies to remap spared inputs around a scotoma or a cortical infarct.

Homeostatic control of interocular balance revealed with contrast mismatch

Short-term monocular deprivation (STMD), wherein one eye is deprived of input for 1–3 hours, induces a temporary (30–60mins) shift in interocular balance. Surprisingly the deprived eye (DE) gets relatively stronger post-deprivation in comparison to the non-deprived eye. STMD may be viewed as presenting an interocular contrast mismatch where one eye (DE) receives a lower contrast than the other. What if the contrast imbalance is in the opposite direction, a contrast increment relative to baseline? Is the STMD effect symmetrical? Primate V1 was optically imaged for ocular dominance columns (ODCs) starting with a baseline of 40% contrast sine gratings of four orientation to each eye. Then the left (manipulated) eye (ME) was switched to 80% contrast, back to 40%, then to 20%, then back to 40% while the right eye was constantly stimulated with 40% (each period lasted for 1–2 hours). Line profiles across the ODCs show DC offset shifts indicative of the relative strength of each eye’s response. The result is that the response to the ME stimuli at first is commensurate with the contrast change, but later begins to shift to match the fellow eye. Whenever the ME returns to baseline (40%), the response “overshoots” or “undershoots” DC zero implying a relative gain change that opposes the previous contrast imbalance. This behavior indicates a binocularly-regulated interocular balancing mechanism, with a time constant of ~30mins. An additional analysis that examines the peak-peak amplitude of the ODC signal shows a companion result, supporting the notion of a binocular homeostatic mechanism regulating interocular balance. Although this STMD gain shift effect was approximately symmetrical, there was an asymmetry such that the 40–80 increment yielded a larger gain shift than the 40-20 decrement. A variant of the DSKL model for binocular combination replicates key features of these interocular contrast imbalance responses.

Lateral geniculate neurons projecting to primary visual cortex show ocular dominance plasticity in adult mice.

Experience-dependent plasticity in the mature visual system is widely considered to be cortical. Using chronic two-photon Ca2+ imaging of thalamic afferents in layer 1 of binocular visual cortex, we provide evidence against this tenet: the respective dorsal lateral geniculate nucleus (dLGN) cells showed pronounced ocular dominance (OD) shifts after monocular deprivation in adult mice. Most (86%), but not all, of dLGN cell boutons were monocular during normal visual experience. Following deprivation, initially deprived-eye-dominated boutons reduced or lost their visual responsiveness to that eye and frequently became responsive to the non-deprived eye. This cannot be explained by eye-specific cortical changes propagating to dLGN via cortico-thalamic feedback because the shift in dLGN responses was largely resistant to cortical inactivation using the GABAA receptor agonist muscimol. Our data suggest that OD shifts observed in the binocular visual cortex of adult mice may at least partially reflect plasticity of eye-specific inputs onto dLGN neurons.

Recovery from the anatomical effects of long‐term monocular deprivation in cat lateral geniculate nucleus

Monocular deprivation (MD) imposed early in postnatal life elicits profound structural and functional abnormalities throughout the primary visual pathway. The ability of MD to modify neurons within the visual system is restricted to a so-called critical period that, for cats, peaks at about one postnatal month and declines thereafter so that by about 3 months of age MD has little effect. Recovery from the consequences of MD likewise adheres to a critical period that ends by about 3 months of age, after which the effects of deprivation are thought to be permanent and without capacity for reversal. The attenuation of plasticity beyond early development is a formidable obstacle for conventional therapies to stimulate recovery from protracted visual deprivation. In the current study we examined the efficacy of dark exposure and retinal inactivation with tetrodotoxin to promote anatomical recovery in the dorsal lateral geniculate nuclues (dLGN) from long-term MD started at the peak of the critical period. Whereas 10 days of dark exposure or binocular retinal inactivation were not better at promoting recovery than conventional treatment with reverse occlusion, inactivation of only the non-deprived (fellow) eye for 10 days produced a complete restoration of neuron soma size, and also reversed the significant loss of neurofilament protein within originally deprived dLGN layers. These results reveal a capacity for neural plasticity and recovery that is larger than anything previously observed following protracted MD in cat, and they highlight a possibility for alternative therapies applied at ages thought to be recalcitrant to recovery.