scholarly journals Cross-modal restoration of juvenile-like ocular dominance plasticity after increasing GABAergic inhibition

2018 ◽  
Author(s):  
Manuel Teichert ◽  
Marcel Isstas ◽  
Franziska Wieske ◽  
Christine Winter ◽  
Jürgen Bolz
Keyword(s):  
Young Adult ◽  
Critical Period ◽  
Hplc Analysis ◽  
Ocular Dominance ◽  
Monocular Deprivation ◽  
Gabaergic Inhibition ◽  
Ocular Dominance Plasticity ◽  
Intrinsic Signal ◽  
Adult Mice ◽  
Contralateral Eye

AbstractIn juvenile and “young adult” mice monocular deprivation (MD) shifts the ocular dominance (OD) of binocular neurons in the primary visual cortex (V1) away from the deprived eye. However, OD plasticity is completely absent in mice older than 110 days, but can be reactivated by treatments which decrease GABA levels in V1. Typically, these OD shifts can be prevented by increasing GABAergic transmission with diazepam. We could recently demonstrate that both bilateral whisker and auditory deprivation (WD, AD), can also restore OD plasticity in mice older than 110 days, since MD for 7 days in WD mice caused a potentiation of V1 input through the ipsilateral (open) eye, the characteristic feature of OD plasticity of “young adult” mice. Here we examined whether WD for 7 days also decreases GABA levels. For this, we performed post mortem HPLC analysis of V1 tissue. Indeed, we found that WD significantly decreased GABA levels in V1. Surprisingly, enhancing GABAergic inhibition by diazepam did not abolish OD shifts in WD mice, as revealed by repeated intrinsic signal imaging. On the contrary, this treatment led to a depression of V1 input through the previously closed contralateral eye, the characteristic signature of OD plasticity in juvenile mice during the critical period. Interestingly, the same result was obtained after AD. Taken together, these results suggest that cross-modally restored OD plasticity does not only depend on reduction of GABA levels in V1, but also requires other, so far unknown mechanisms.

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.

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.

Layer differences in the effect of monocular vision in light- and dark-reared kittens

2001 ◽  
Vol 18 (5) ◽  
pp. 811-820 ◽  
Author(s):  
CHRISTOPHER J. BEAVER ◽  
QINGHUA JI ◽  
NIGEL W. DAW
Keyword(s):  
Visual Cortex ◽  
Critical Period ◽  
Ocular Dominance ◽  
Large Change ◽  
Monocular Deprivation ◽  
Monocular Vision ◽  
Ocular Dominance Plasticity ◽  
The Difference ◽  
Dark Rearing

We compared the effect of 2 days of monocular vision on the ocular dominance of cells in the visual cortex of light-reared kittens with the effect in dark-reared kittens at 6, 9, and 14 weeks of age, and analyzed the results by layer. The size of the ocular-dominance shift declined with age in all layers in light-reared animals. There was not a large change in the ocular-dominance shift with age in dark-reared animals in any layer, suggesting that dark rearing largely keeps the cortex in the immature 6-week state until 14 weeks or longer, although there was a slight decrease in layers II, III, and IV, and a slight increase in layers V and VI. At 14 weeks, the difference between light- and dark-reared animals was smallest in layer IV, larger in layers II/III, and largest in layers V/VI, suggesting that dark rearing has a large effect on intracortical synapses and a small effect on geniculocortical synapses. There was a significant ocular-dominance shift in layer IV at 14 weeks of age in both light- animals and dark-reared animals, showing that the critical period for ocular-dominance plasticity is not ended at this age. While the ocular-dominance shift after 26 h of monocular deprivation in 6-week animals was similar in light- and dark-reared animals, after 14 h it was smaller in dark-reared animals, showing that ocular-dominance changes occur more slowly in dark-reared animals at this age, in agreement with Mower (1991). Increases in selectivity for axis of movement after 26 h of monocular vision were seen in dark-reared animals at 6 weeks of age, but not at 9 or 14 weeks of age, showing that the critical period for axial selectivity ends earlier than the critical period for ocular dominance in dark-reared animals, as it does in light-reared animals.

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’.

scholarly journals Astrocytic glutamate uptake coordinates experience-dependent, eye-specific refinement in developing visual cortex

2020 ◽  
Author(s):  
Grayson Sipe ◽  
Jeremy Petravicz ◽  
Rajeev Rikhye ◽  
Rodrigo Garcia ◽  
Nikolaos Mellios ◽  
...  
Keyword(s):  
Visual Cortex ◽  
Glutamate Uptake ◽  
Ocular Dominance ◽  
Glutamate Transporter ◽  
Monocular Deprivation ◽  
Spine Density ◽  
Ocular Dominance Plasticity ◽  
Contralateral Eye ◽  
Cortical Inputs ◽  
And Function

ABSTRACTThe uptake of glutamate by astrocytes actively shapes synaptic transmission, however its role in the development and plasticity of neuronal circuits remains poorly understood. The astrocytic glutamate transporter, GLT1 is the predominant source of glutamate clearance in the adult mouse cortex. Here, we examined the structural and functional development of the visual cortex in GLT1 heterozygous (HET) mice using two-photon microscopy, immunohistochemistry and slice electrophysiology. We find that though eye-specific thalamic axonal segregation is intact, binocular refinement in the primary visual cortex is disrupted. Eye-specific responses to visual stimuli in GLT1 HET mice show altered binocular matching, with abnormally high responses to ipsilateral compared to contralateral eye stimulation and a greater mismatch between preferred orientation selectivity of ipsilateral and contralateral eye responses. Furthermore, the balance of excitation and inhibition in cortical circuits is dysregulated with an increase in somatostatin positive interneurons, decrease in parvalbumin positive interneurons, and increase in dendritic spine density in the basal dendrites of layer 2/3 excitatory neurons. Monocular deprivation induces atypical ocular dominance plasticity in GLT1 HET mice, with an unusual depression of ipsilateral open eye responses; however, this change in ipsilateral responses correlates well with an upregulation of GLT1 protein following monocular deprivation. These results demonstrate that a key function of astrocytic GLT1 function during development is the experience-dependent refinement of ipsilateral eye inputs relative to contralateral eye inputs in visual cortex.SIGNIFICANCEWe show that astrocytic glutamate uptake via the transporter GLT1 is necessary for activity-dependent regulation of cortical inputs. Dysregulation of GLT1 expression and function leads to a disruption of binocular refinement and matching in visual cortex. Inputs from the ipsilateral eye are stronger, and monocular deprivation, which upregulates GLT1 expression in a homeostatic fashion, causes a paradoxical reduction of ipsilateral, non-deprived eye, responses. These results provide new evidence for the importance of glutamate transport in cortical development, function, and plasticity.

scholarly journals All-or-none disconnection of pyramidal inputs onto parvalbumin-positive interneurons gates ocular dominance plasticity

2021 ◽  
Author(s):  
Daniel Severin ◽  
Su Z. Hong ◽  
Seung-Eon Roh ◽  
Jiechao Zhou ◽  
Michelle C. D. Bridi ◽  
...  
Keyword(s):  
Critical Period ◽  
Cortical Plasticity ◽  
Classical Model ◽  
Ocular Dominance ◽  
Pyramidal Cells ◽  
Initial Step ◽  
Monocular Deprivation ◽  
Ocular Dominance Plasticity ◽  
Reversible Loss ◽  
Underlying Mechanisms

ABSTRACTDisinhibition is an obligatory initial step in the remodeling of cortical circuits by sensory experience, yet the underlying mechanisms remain unclear. Our investigation of mechanisms for disinhibition in the classical model of ocular dominance plasticity (ODP) uncovered an unexpected novel form of experience-dependent circuit plasticity. In layer 2/3 of mouse visual cortex monocular deprivation triggers an “all-or-none” elimination of approximately half the connections from local pyramidal cells onto parvalbumin-positive interneurons (Pyr→PV), without affecting the strength of the remaining connections. This loss of Pyr→PV connections is transient, lasting one day only, has a critical period commensurate with the ODP critical period, and is contingent on a reduction of neuropentraxin2 (NPTX2), which normally stabilizes Pyr→PV connections. Bidirectional manipulations of NPTX2 functionality that prevent/promote the elimination Pyr→PV connections also promote/prevent ODP. We surmise, therefore, that this rapid and reversible loss of local Pyr→PV circuitry gates experience-dependent cortical plasticity.

GAP-43 in the cat visual cortex during postnatal development

1990 ◽  
Vol 4 (6) ◽  
pp. 585-593 ◽  
Author(s):  
Helen McIntosh ◽  
Nigel Daw ◽  
David Parkinson
Keyword(s):  
Visual Cortex ◽  
Postnatal Development ◽  
Critical Period ◽  
Primary Motor Cortex ◽  
Ocular Dominance ◽  
Monocular Deprivation ◽  
Ocular Dominance Plasticity ◽  
Cat Visual Cortex ◽  
Age Gap ◽  
Slow Decline

AbstractGAP-43 levels have been determined by immunoassay in cat visual cortex during postnatal development to test the idea that GAP-43 expression could be related to the duration of the critical period for plasticity. For comparison, GAP-43 levels have also been assayed in primary motor cortex, primary somatosensory cortex, and cerebellum at each age. GAP-43 levels were high in all regions at 5 d (with concentrations ranging from 7−10 ng;/μg protein) and then declined 60−80% by 60 d of age. After 60 d of age, GAP-43 concentrations in each region continued a slow decline to adult values, which ranged from 0.5−2 ng/μg protein. To test for the involvement of GAP-43 in ocular dominance plasticity during the critical period, the effect of visual deprivation on GAP-43 levels was investigated. Monocular deprivation for 2−7 d, ending at either 27 or 35 d of age, had no effect on total membrane levels of GAP-43. The concentrations of membrane-associated GAP-43 prior to 40 d of age correlate with events that occur during postnatal development of the cat visual cortex. However, the slow decline in membrane-associated GAP-43 levels after 40 d of age may be an index of relative plasticity remaining after the peak of the critical period.

scholarly journals Visual deprivation independent shift of ocular dominance induced by cross-modal plasticity

2018 ◽  
Author(s):  
Manuel Teichert ◽  
Marcel Isstas ◽  
Lutz Liebmann ◽  
Christian A. Hübner ◽  
Franziska Wieske ◽  
...  
Keyword(s):  
Visual Experience ◽  
Late Onset ◽  
Ocular Dominance ◽  
Sensory Modality ◽  
Convincing Evidence ◽  
Intrinsic Signal ◽  
Adult Mice ◽  
Layer 4 ◽  
Sensory Cortices ◽  
Contralateral Eye

AbstractThere is convincing evidence that the deprivation of one sense can lead to adaptive neuronal changes in the spared primary sensory cortices. However, the repercussions of late-onset sensory deprivations on functionality of the remaining sensory cortices are poorly understood. Using repeated intrinsic signal imaging we investigated the effects of whisker or auditory deprivation (WD or AD, respectively) on responsiveness of the binocular primary visual cortex (V1) in fully adult mice. The binocular zone of mice is innervated by both eyes, with the contralateral eye always dominating V1 input over ipsilateral eye input, the normal ocular dominance (OD) ratio. Strikingly, we found that 3 days after WD or AD there was a transient shift of OD, which was mediated by a potentiation of V1 input through the ipsilateral eye. This cross-modal effect was accompanied by strengthening of V1 layer 4 synapses, required visual experience through the ipsilateral eye and was mediated by an increase of the excitation/inhibition ratio in V1. Finally, we demonstrate that both WD and AD induced a long-lasting improvement of visual performance. Our data provide evidence that the deprivation of a non-visual sensory modality cross-modally induces experience dependent V1 plasticity and improves visual behavior, even in adult mice.

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.

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