scholarly journals Modification of Peak Plasticity Induced by Brief Dark Exposure

2019 ◽  
Vol 2019 ◽  
pp. 1-10
Author(s):  
Alexander J. Lingley ◽  
Donald E. Mitchell ◽  
Nathan A. Crowder ◽  
Kevin R. Duffy
Keyword(s):  
Visual System ◽  
Neural Plasticity ◽  
Critical Period ◽  
Ocular Dominance ◽  
Monocular Deprivation ◽  
Dorsal Lateral Geniculate Nucleus ◽  
Soma Size ◽  
Slow Progress ◽  
Dark Exposure ◽  
Central Visual System

The capacity for neural plasticity in the mammalian central visual system adheres to a temporal profile in which plasticity peaks early in postnatal development and then declines to reach enduring negligible levels. Early studies to delineate the critical period in cats employed a fixed duration of monocular deprivation to measure the extent of ocular dominance changes induced at different ages. The largest deprivation effects were observed at about 4 weeks postnatal, with a steady decline in plasticity thereafter so that by about 16 weeks only small changes were measured. The capacity for plasticity is regulated by a changing landscape of molecules in the visual system across the lifespan. Studies in rodents and cats have demonstrated that the critical period can be altered by environmental or pharmacological manipulations that enhance plasticity at ages when it would normally be low. Immersion in complete darkness for long durations (dark rearing) has long been known to alter plasticity capacity by modifying plasticity-related molecules and slowing progress of the critical period. In this study, we investigated the possibility that brief darkness (dark exposure) imposed just prior to the critical period peak can enhance the level of plasticity beyond that observed naturally. We examined the level of plasticity by measuring two sensitive markers of monocular deprivation, namely, soma size of neurons and neurofilament labeling within the dorsal lateral geniculate nucleus. Significantly larger modification of soma size, but not neurofilament labeling, was observed at the critical period peak when dark exposure preceded monocular deprivation. This indicated that the natural plasticity ceiling is modifiable and also that brief darkness does not simply slow progress of the critical period. As an antecedent to traditional amblyopia treatment, darkness may increase treatment efficacy even at ages when plasticity is at its highest.

Short periods of darkness fail to restore visual or neural plasticity in adult cats

2018 ◽  
Vol 35 ◽  
Author(s):  
KAITLYN D. HOLMAN ◽  
KEVIN R. DUFFY ◽  
DONALD E. MITCHELL
Keyword(s):  
Visual Acuity ◽  
Neural Plasticity ◽  
Early Period ◽  
Monocular Deprivation ◽  
Dorsal Lateral Geniculate Nucleus ◽  
Soma Size ◽  
Visual Acuity Loss ◽  
Adult Cats ◽  
One Year ◽  
Dorsal Lateral Geniculate

AbstractIt has been shown that the visual acuity loss experienced by the deprived eye of kittens following an early period of monocular deprivation (MD) can be alleviated rapidly following 10 days of complete darkness when imposed even as late as 14 weeks of age. To examine whether 10 days of darkness conferred benefits at any age, we measured the extent of recovery of the visual acuity of the deprived eye following the darkness imposed on adult cats that had received the same early period of MD as used in prior experiments conducted on kittens. Parallel studies conducted on different animals examined the extent to which darkness changed the magnitude of the MD-induced laminar differences of the cell soma size and immunoreactivity for the neurofilament (NF) protein in the dorsal lateral geniculate nucleus (dLGN). The results indicated that 10 days of darkness imposed at one year of age neither alleviated the acuity loss of the deprived eye induced by an earlier period of MD nor did it decrease the concurrent lamina differences of the soma size or NF loss in the dLGN.

scholarly journals Light reintroduction after dark exposure reactivates plasticity in adults via perisynaptic activation of MMP-9

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Sachiko Murase ◽  
Crystal L Lantz ◽  
Elizabeth M Quinlan
Keyword(s):  
Critical Period ◽  
Adult Mouse ◽  
Ocular Dominance ◽  
Visual Deprivation ◽  
Monocular Deprivation ◽  
Genetic Ablation ◽  
Dark Exposure ◽  
Cortical Synapses ◽  
Mouse Visual Cortex ◽  
Metalloproteinase 9

The sensitivity of ocular dominance to regulation by monocular deprivation is the canonical model of plasticity confined to a critical period. However, we have previously shown that visual deprivation through dark exposure (DE) reactivates critical period plasticity in adults. Previous work assumed that the elimination of visual input was sufficient to enhance plasticity in the adult mouse visual cortex. In contrast, here we show that light reintroduction (LRx) after DE is responsible for the reactivation of plasticity. LRx triggers degradation of the ECM, which is blocked by pharmacological inhibition or genetic ablation of matrix metalloproteinase-9 (MMP-9). LRx induces an increase in MMP-9 activity that is perisynaptic and enriched at thalamo-cortical synapses. The reactivation of plasticity by LRx is absent in Mmp9−/− mice, and is rescued by hyaluronidase, an enzyme that degrades core ECM components. Thus, the LRx-induced increase in MMP-9 removes constraints on structural and functional plasticity in the mature cortex.

scholarly journals Axonal processes and neural plasticity. III. Competition for dendrites

1997 ◽  
Vol 352 (1364) ◽  
pp. 1975-1983 ◽  
Author(s):  
T. Elliott ◽  
C. I. Howarth ◽  
N. R. Shadbolt
Keyword(s):  
Neural Plasticity ◽  
Critical Period ◽  
Ocular Dominance ◽  
Dendritic Morphology ◽  
Monocular Deprivation ◽  
Topographic Map ◽  
Cortical Cells ◽  
Optic Nerve Stimulation ◽  
Axonal Process ◽  
Dendritic Fields

In previous work we have developed a computational framework for topographic map formation and plasticity based on axonal process sprouting and retraction, in which sprouting and retraction are governed by competition for neurotrophic support. Here we show that such an approach can account for certain aspects of the dendritic morphology of cortical maps. In particular, we model the development of ocular dominance columns in the primary visual cortex and show that cortical cells near to column boundaries prefer to elaborate dendritic fields which avoid crossing the boundaries. This emerges as different functional inputs are spatially separated. We predict that afferent segregation occurs before or simultaneously with, but not after, the emergence of dendritic bias. We predict that animals reared with complete but asynchronous stimulation of the optic nerves do not develop a dendritic bias. We suggest that the emergence of a dendritic bias might provide a partial account for the critical period for a response to monocular deprivation. In particular, we predict that animals reared with asynchronous optic nerve stimulation might exhibit an extended critical period. Our results also indicate that the number of synapses supported by cortical cells depends on the intra–ocular image correlations used in our simulations. This suggests that inter–ocular image correlations, and thus strabismic rearing of kittens, may also affect the innervation density.

Recovery of Cortical Binocularity and Orientation Selectivity After the Critical Period for Ocular Dominance Plasticity

2004 ◽  
Vol 92 (4) ◽  
pp. 2113-2121 ◽  
Author(s):  
David S. Liao ◽  
Thomas E. Krahe ◽  
Glen T. Prusky ◽  
Alexandre E. Medina ◽  
Ary S. Ramoa
Keyword(s):  
Binocular Vision ◽  
Neural Plasticity ◽  
Critical Period ◽  
Visual Experience ◽  
Ocular Dominance ◽  
Orientation Selectivity ◽  
Monocular Deprivation ◽  
Ocular Dominance Plasticity ◽  
Single Unit Recordings ◽  
Normal Binocular Vision

Cortical binocularity is abolished by monocular deprivation (MD) during a critical period of development lasting from approximately postnatal day (P) 35 to P70 in ferrets. Although this is one of the best-characterized models of neural plasticity and amblyopia, very few studies have examined the requirements for recovery of cortical binocularity and orientation selectivity of deprived eye responses. Recent studies indicating that different mechanisms regulate loss and recovery of binocularity raise the possibility that different sensitive periods characterize loss and recovery of deprived eye responses. In this report, we have examined whether the potential for recovery of binocularity and orientation selectivity is restricted to the critical period. Quantitative single unit recordings revealed recovery of cortical binocularity and full recovery of orientation selectivity of deprived eye responses following prolonged periods of MD (i.e., >3 wk) starting at P49, near the peak of plasticity. Surprisingly, recovery was present when binocular vision was restored after the end of the critical period for ocular dominance plasticity, as late as P83. In contrast, ferrets that had never received visual experience through the deprived eye failed to recover binocularity even though normal binocular vision was restored at P50, halfway through the critical period. Collectively, these results indicate that there is potential for recovery of cortical binocularity and deprived eye orientation selectivity after the end of the critical period for ocular dominance plasticity.

scholarly journals Enhancement of visual cortex plasticity by dark exposure

2017 ◽  
Vol 372 (1715) ◽  
pp. 20160159 ◽  
Author(s):  
Irina Erchova ◽  
Asta Vasalauskaite ◽  
Valentina Longo ◽  
Frank Sengpiel
Keyword(s):  
Visual Cortex ◽  
Critical Period ◽  
Time Course ◽  
Ocular Dominance ◽  
Monocular Deprivation ◽  
Homeostatic Plasticity ◽  
Ocular Dominance Plasticity ◽  
Intrinsic Signals ◽  
Significant Difference ◽  
Dark Exposure

Dark rearing is known to delay the time course of the critical period for ocular dominance plasticity in the visual cortex. Recent evidence suggests that a period of dark exposure (DE) may enhance or reinstate plasticity even after closure of the critical period, mediated through modification of the excitatory–inhibitory balance and/or removal of structural brakes on plasticity. Here, we investigated the effects of a week of DE on the recovery from a month of monocular deprivation (MD) in the primary visual cortex (V1) of juvenile mice. Optical imaging of intrinsic signals revealed that ocular dominance in V1 of mice that had received DE recovered slightly more quickly than of mice that had not, but the level of recovery after three weeks was similar in both groups. Two-photon calcium imaging showed no significant difference in the recovery of orientation selectivity of excitatory neurons between the two groups. Parvalbumin-positive (PV+) interneurons exhibited a smaller ocular dominance shift during MD but again no differences in subsequent recovery. The percentage of PV+ cells surrounded by perineuronal nets, a structural brake on plasticity, was lower in mice with than those without DE. Overall, DE causes a modest enhancement of mouse visual cortex plasticity. This article is part of the themed issue ‘Integrating Hebbian and homeostatic plasticity’.

Critical period for monocular deprivation in the cat visual cortex

1992 ◽  
Vol 67 (1) ◽  
pp. 197-202 ◽  
Author(s):  
N. W. Daw ◽  
K. Fox ◽  
H. Sato ◽  
D. Czepita
Keyword(s):  
Visual Cortex ◽  
Critical Period ◽  
Single Cells ◽  
Ocular Dominance ◽  
Monocular Deprivation ◽  
Significant Shift ◽  
Cat Visual Cortex

1. Cats were monocularly deprived for 3 mo starting at 8-9 mo, 12 mo, 15 mo, and several years of age. Single cells were recorded in both visual cortexes of each cat, and the ocular dominance and layer determined for each cell. Ocular dominance histograms were then constructed for layers II/III, IV, and V/VI for each group of animals. 2. There was a statistically significant shift in the ocular dominance for cells in layers II/III and V/VI for the animals deprived between 8-9 and 11-12 mo of age. There was a small but not statistically significant shift for cells in layer IV from the animals deprived between 8-9 and 11-12 mo of age, and for cells in layers V/VI from the animals deprived between 15 and 18 mo of age. There was no noticeable shift in ocular dominance for any other layers in any other group of animals. 3. We conclude that the critical period for monocular deprivation is finally over at approximately 1 yr of age for extragranular layers (layers II, III, V, and VI) in visual cortex of the cat.

scholarly journals Critical periods in amblyopia

2018 ◽  
Vol 35 ◽  
Author(s):  
TAKAO K. HENSCH ◽  
ELIZABETH M. QUINLAN
Keyword(s):  
Visual Cortex ◽  
Critical Period ◽  
Molecular Mechanisms ◽  
Ocular Dominance ◽  
Molecular Genetic ◽  
Monocular Deprivation ◽  
Critical Periods ◽  
Developmental Constraints ◽  
Early Postnatal Development ◽  
Visual Cortical

AbstractThe shift in ocular dominance (OD) of binocular neurons induced by monocular deprivation is the canonical model of synaptic plasticity confined to a postnatal critical period. Developmental constraints on this plasticity not only lend stability to the mature visual cortical circuitry but also impede the ability to recover from amblyopia beyond an early window. Advances with mouse models utilizing the power of molecular, genetic, and imaging tools are beginning to unravel the circuit, cellular, and molecular mechanisms controlling the onset and closure of the critical periods of plasticity in the primary visual cortex (V1). Emerging evidence suggests that mechanisms enabling plasticity in juveniles are not simply lost with age but rather that plasticity is actively constrained by the developmental up-regulation of molecular ‘brakes’. Lifting these brakes enhances plasticity in the adult visual cortex, and can be harnessed to promote recovery from amblyopia. The reactivation of plasticity by experimental manipulations has revised the idea that robust OD plasticity is limited to early postnatal development. Here, we discuss recent insights into the neurobiology of the initiation and termination of critical periods and how our increasingly mechanistic understanding of these processes can be leveraged toward improved clinical treatment of adult amblyopia.

Orientation Selectivity Is Reduced by Monocular Deprivation in Combination With PKA Inhibitors

2002 ◽  
Vol 88 (4) ◽  
pp. 1933-1940 ◽  
Author(s):  
Chris J. Beaver ◽  
Quentin S. Fischer ◽  
Qinghua Ji ◽  
Nigel W. Daw
Keyword(s):  
Visual Cortex ◽  
Protein Kinase ◽  
Critical Period ◽  
Ocular Dominance ◽  
Receptive Fields ◽  
Direction Selectivity ◽  
Orientation Selectivity ◽  
Monocular Deprivation ◽  
Ocular Dominance Plasticity ◽  
Kinase A

We have previously shown that the protein kinase A (PKA) inhibitor, 8-chloroadenosine-3′,5′–monophosphorothioate (Rp-8-Cl-cAMPS), abolishes ocular dominance plasticity in the cat visual cortex. Here we investigate the effect of this inhibitor on orientation selectivity. The inhibitor reduces orientation selectivity in monocularly deprived animals but not in normal animals. In other words, PKA inhibitors by themselves do not affect orientation selectivity, nor does monocular deprivation by itself, but monocular deprivation in combination with a PKA inhibitor does affect orientation selectivity. This result is found for the receptive fields in both deprived and nondeprived eyes. Although there is a tendency for the orientation selectivity in the nondeprived eye to be higher than the orientation selectivity in the deprived eye, the orientation selectivity in both eyes is considerably less than normal. The result is striking in animals at 4 wk of age. The effect of the monocular deprivation on orientation selectivity is reduced at 6 wk of age and absent at 9 wk of age, while the effect on ocular dominance shifts is less changed in agreement with previous results showing that the critical period for orientation/direction selectivity ends earlier than the critical period for ocular dominance. We conclude that closure of one eye in combination with inhibition of PKA reduces orientation selectivity during the period that orientation selectivity is still mutable and that the reduction in orientation selectivity is transferred to the nondeprived eye.

scholarly journals Lateral geniculate neurons show robust ocular dominance plasticity

2017 ◽  
Author(s):  
Juliane Jäpel ◽  
Mark Hübener ◽  
Tobias Bonhoeffer ◽  
Tobias Rose
Keyword(s):  
Visual Cortex ◽  
Visual System ◽  
Ocular Dominance ◽  
Monocular Deprivation ◽  
Ocular Dominance Plasticity ◽  
Dependent Plasticity ◽  
Two Photon ◽  
Lateral Geniculate

AbstractExperience-dependent plasticity in the mature visual system is considered exclusively cortical. Using chronic two-photon Ca2+ imaging, we found evidence against this tenet: dLGN cells showed robust ocular dominance shifts after monocular deprivation. Most, but not all responses of dLGN cell boutons in binocular visual cortex were monocular during baseline. Following deprivation, however, deprived-eye dominated boutons became responsive to the non-deprived eye. Thus, plasticity of dLGN neurons contributes to cortical ocular dominance shifts.

Possible Role of Corticosteroids in Nervous System Plasticity: Improvement in Amblyopia After Optic Neuritis in the Fellow Eye Treated with Steroids

2001 ◽  
Vol 15 (3) ◽  
pp. 223-227 ◽  
Author(s):  
Cris S. Constantinescu ◽  
Irene Gottlob
Keyword(s):  
Visual System ◽  
Optic Neuritis ◽  
Neural Plasticity ◽  
Critical Period ◽  
Visual Stimulation ◽  
High Dose ◽  
Fellow Eye ◽  
Visual Improvement ◽  
Contralateral Eye

Objective: Amblyopia consists of reduced visual function in the absence of or ganic disease, caused by deficient visual stimulation, most commonly due to squint or refractive error. Amblyopia is thought to be reversible up until the age of ∼8 years (critical period) and is usually treated with occlusion of the fellow eye. There is re cent evidence for visual system plasticity extending beyond the critical period, sup ported by reports of improvement in visual acuity in the amblyopic eye after loss of vision in the contralateral eye. This suggests that the adult visual system exhibits suf ficient plasticity to allow such improvement. We describe here improvement in vi sual acuity in three amblyopic patients after they received high-dose intravenous glu cocorticoids for optic neuritis in the contralateral eye. Methods: Clinical and neurological evaluation added. Results: In all cases, the improvement was sustained, even after the recovery from the optic neuritis. Conclusions: Because steroids affect neural plasticity, we hypothesize that they facilitate and enhance visual improvement in amblyopia, a quality that may be tested in future controlled trials. Key Words: Am biyopia—Steroids—Plasticity—Glucocorticoids—Optic neuritis.

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