scholarly journals Recovery of glutamatergic and GABAergic protein expression in visual cortex after monocular deprivation

2019 ◽  
Author(s):  
Justin L. Balsor ◽  
David G. Jones ◽  
Kathryn M. Murphy
Keyword(s):  
Visual Cortex ◽  
Protein Expression ◽  
Binocular Vision ◽  
Critical Period ◽  
Visual Experience ◽  
Monocular Deprivation ◽  
The Other ◽  
Synaptic Proteins ◽  
Normal Expression ◽  
Binocular Deprivation

AbstractA collection of glutamatergic and GABAergic proteins participate in regulating experience-dependent plasticity in the visual cortex (V1). Many studies have characterized changes to those proteins caused by monocular deprivation (MD) during the critical period (CP), but less is known about changes that occur when MD stops. We measured the effects of 3 types of visual experience after MD (n=24, 10 male and 14 female); reverse occlusion (RO), binocular deprivation (BD), or binocular vision, on the expression of synaptic proteins in V1 including glutamatergic and GABAergic receptor subunits. Synapsin expression was increased by RO but not affected by the other treatments. BD shifted the balance between glutamatergic and GABAergic receptor subunits to favor GABAAα1. In contrast, BV shifted expression to favor the glutamatergic mechanisms by increasing NMDAR and decreasing GABAAα1 subunits. None of the conditions returned normal expression levels to all of the proteins, but BV was the closest.

scholarly journals Classification of visual cortex plasticity phenotypes following treatment for amblyopia

2019 ◽  
Author(s):  
Justin L. Balsor ◽  
David G. Jones ◽  
Kathryn M. Murphy
Keyword(s):  
Visual Cortex ◽  
Critical Period ◽  
Monocular Deprivation ◽  
Data Driven ◽  
Adaptive Plasticity ◽  
Gabaergic Receptors ◽  
Data Driven Approach ◽  
Binocular Deprivation ◽  
Induced Changes

AbstractMonocular deprivation (MD) during the critical period (CP) has enduring effects on visual acuity and the functioning of the visual cortex (V1). This experience-dependent plasticity has become a model for studying the mechanisms, especially glutamatergic and GABAergic receptors, that regulate amblyopia. Less is known, however, about treatment-induced changes to those receptors and if those changes differentiate treatments that support the recovery of acuity versus persistent acuity deficits. Here we use an animal model to explore the effects of 3 visual treatments started during the CP (n=24, 10 male and 14 female); binocular vision (BV) that promotes good acuity versus reverse occlusion (RO) and binocular deprivation (BD) that causes persistent acuity deficits. We measured recovery of a collection of glutamatergic and GABAergic receptor subunits in V1 and modeled recovery of kinetics for NMDAR and GABAAR. There was a complex pattern of protein changes that prompted us to develop an unbiased data-driven approach for these high-dimensional data analyses to identify plasticity features and construct plasticity phenotypes. Cluster analysis of the plasticity phenotypes suggests that BV supports adaptive plasticity while RO and BD promote a maladaptive pattern. The RO plasticity phenotype appeared more similar to adults with high expression of GluA2 and the BD phenotypes were dominated by GABAAα1, highlighting that multiple plasticity phenotypes can underlie persistent poor acuity. After 2-4 days of BV the plasticity phenotypes resembled normals, but only one feature, the GluN2A:GluA2 balance, returned to normal levels. Perhaps, balancing Hebbian (GluN2A) and homeostatic (GluA2) mechanisms is necessary for the recovery of vision.

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 Sensory experience inversely regulates feedforward and feedback excitation-inhibition ratio in rodent visual cortex

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Nathaniel J Miska ◽  
Leonidas MA Richter ◽  
Brian A Cary ◽  
Julijana Gjorgjieva ◽  
Gina G Turrigiano
Keyword(s):  
Visual Cortex ◽  
Driving Force ◽  
Critical Period ◽  
Visual Experience ◽  
Feedback Inhibition ◽  
Intracortical Inhibition ◽  
Monocular Deprivation ◽  
Long Term Depression ◽  
Layer 4

Brief (2-3d) monocular deprivation (MD) during the critical period induces a profound loss of responsiveness within binocular (V1b) and monocular (V1m) regions of rodent primary visual cortex. This has largely been ascribed to long-term depression (LTD) at thalamocortical synapses, while a contribution from intracortical inhibition has been controversial. Here we used optogenetics to isolate and measure feedforward thalamocortical and feedback intracortical excitation-inhibition (E-I) ratios following brief MD. Despite depression at thalamocortical synapses, thalamocortical E-I ratio was unaffected in V1b and shifted toward excitation in V1m, indicating that thalamocortical excitation was not effectively reduced. In contrast, feedback intracortical E-I ratio was shifted toward inhibition in V1m, and a computational model demonstrated that these opposing shifts produced an overall suppression of layer 4 excitability. Thus, feedforward and feedback E-I ratios can be independently tuned by visual experience, and enhanced feedback inhibition is the primary driving force behind loss of visual responsiveness.

scholarly journals Classification of Visual Cortex Plasticity Phenotypes following Treatment for Amblyopia

2019 ◽  
Vol 2019 ◽  
pp. 1-23 ◽  
Author(s):  
Justin L. Balsor ◽  
David G. Jones ◽  
Kathryn M. Murphy
Keyword(s):  
Visual Cortex ◽  
Critical Period ◽  
Monocular Deprivation ◽  
Data Driven ◽  
Adaptive Plasticity ◽  
Gabaergic Receptors ◽  
Data Driven Approach ◽  
Binocular Deprivation ◽  
Induced Changes

Monocular deprivation (MD) during the critical period (CP) has enduring effects on visual acuity and the functioning of the visual cortex (V1). This experience-dependent plasticity has become a model for studying the mechanisms, especially glutamatergic and GABAergic receptors, that regulate amblyopia. Less is known, however, about treatment-induced changes to those receptors and if those changes differentiate treatments that support the recovery of acuity versus persistent acuity deficits. Here, we use an animal model to explore the effects of 3 visual treatments started during the CP (n=24, 10 male and 14 female): binocular vision (BV) that promotes good acuity versus reverse occlusion (RO) and binocular deprivation (BD) that causes persistent acuity deficits. We measured the recovery of a collection of glutamatergic and GABAergic receptor subunits in the V1 and modeled recovery of kinetics for NMDAR and GABAAR. There was a complex pattern of protein changes that prompted us to develop an unbiased data-driven approach for these high-dimensional data analyses to identify plasticity features and construct plasticity phenotypes. Cluster analysis of the plasticity phenotypes suggests that BV supports adaptive plasticity while RO and BD promote a maladaptive pattern. The RO plasticity phenotype appeared more similar to adults with a high expression of GluA2, and the BD phenotypes were dominated by GABAAα1, highlighting that multiple plasticity phenotypes can underlie persistent poor acuity. After 2-4 days of BV, the plasticity phenotypes resembled normals, but only one feature, the GluN2A:GluA2 balance, returned to normal levels. Perhaps, balancing Hebbian (GluN2A) and homeostatic (GluA2) mechanisms is necessary for the recovery of vision.

scholarly journals Activation of NMDA Receptors Is Necessary for the Recovery of Cortical Binocularity

2010 ◽  
Vol 103 (5) ◽  
pp. 2700-2706 ◽  
Author(s):  
Thomas E. Krahe ◽  
Alexandre E. Medina
Keyword(s):  
Visual Cortex ◽  
Primary Visual Cortex ◽  
Binocular Vision ◽  
Critical Period ◽  
Functional Change ◽  
Monocular Deprivation ◽  
Extracellular Recordings ◽  
Aspartate Receptor ◽  
Critical Period Of Development

Classic experiments have indicated that monocular deprivation (MD) for a few days during a critical period of development results in a decrease in the strength of connections mediating responses to the deprived eye, leading to a dramatic breakdown of cortical neuron binocularity. Despite the substantial functional change in the visual cortex, recovery from the effects of MD can be obtained if binocular vision is promptly restored. While great efforts have been made to elucidate the mechanisms regulating loss of deprived eye function, the mechanisms that underlie the recovery of cortical binocularity are poorly understood. Here, we examined whether activation of the N-methyl-d-aspartate receptor (NMDAR) is required for the recovery of cortical binocularity by pharmacologically blocking the NMDAR using d,l-2-amino-5-phosphonopentanoic (APV). Ferrets ( n = 10) were monocularly deprived for 6 days, and osmotic minipumps, filled with APV (5.6 mg/ml) or saline, were surgically implanted into the primary visual cortex. One day after surgery, the deprived eye was reopened, and the animals were allowed 24 h of binocular vision. Extracellular recordings showed that intracortical infusion of the NMDAR antagonist, APV, prevented recovery of cortical binocularity while preserving neuronal responsiveness. These findings provide an important new insight for a specific role of NMDARs in the recovery of cortical binocularity from the effects of MD.

scholarly journals Experience-dependent development of NMDAR1 subunit expression in the lateral geniculate nucleus

1999 ◽  
Vol 16 (4) ◽  
pp. 781-789 ◽  
Author(s):  
MARK A. FAVA ◽  
KEVIN R. DUFFY ◽  
KATHRYN M. MURPHY
Keyword(s):  
Visual Cortex ◽  
Postnatal Development ◽  
Lateral Geniculate Nucleus ◽  
Critical Period ◽  
Visual Experience ◽  
Monocular Deprivation ◽  
Lateral Geniculate ◽  
Subunit Expression ◽  
Complete Reversal ◽  
Eye Opening

Monocular deprivation early in postnatal development leads to anatomical and physiological changes in the lateral geniculate nucleus (LGN) and visual cortex. Many of these changes are dependent upon activation of the NMDA receptor. We have examined the role of visual experience in modifying NMDAR1 subunit expression in the LGN of animals reared with various forms of visual deprivation. Following monocular deprivation initiated either at eye opening or at the peak of the critical period, there were approximately 20% fewer NMDAR1-immunopositive neurons in the deprived laminae of the LGN. The loss of NMDAR1-immunopositive neurons was found throughout both the binocular and monocular segments of the LGN and after monocular deprivation until just 3 weeks of age. These results indicate that the loss of NMDAR1 in the LGN following monocular deprivation does not simply reflect changes in the visual cortex. The loss of NMDAR1 expression was not necessarily permanent. Initiation of binocular vision at the peak of the critical period ameliorated the effect of monocular deprivation and the introduction of a period of reverse occlusion led to a complete reversal. Taken together, the results show that the expression of the NMDAR1 subunit in the LGN can be modified by the pattern of visual experience during postnatal development.

scholarly journals Protein expression of MEF2C during the critical period for visual development in vervet monkeys

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Daniel M Bernad ◽  
Pascal E Lachance ◽  
Avijit Chaudhuri
Keyword(s):  
Visual Cortex ◽  
Protein Expression ◽  
Critical Period ◽  
Molecular Mechanisms ◽  
Neuronal Survival ◽  
Expression Patterns ◽  
Visual Development ◽  
Monocular Deprivation ◽  
Vervet Monkeys ◽  
Monkey Visual Cortex

During the early development of the visual cortex, there is a critical period when neuronal connections are highly sensitive to changes in visual input. Deprivation of visual stimuli during the critical period elicits robust anatomical and physiological rearrangements in the monkey visual cortex and serves as an excellent model for activity-dependent neuroplasticity. DNA microarray experiments were previously performed in our lab to analyze gene expression patterns in area V1 of vervet monkeys subjected to monocular deprivation (MD). An interesting candidate identified in its screen was myocyte enhancer-binding factor 2C (MEF2C), a transcription factor linked to neuronal survival. Consistent with the microarray data, we show that there is a qualitative increase in MEF2C protein expression in area V1 of infant as compared to adult vervet monkeys. Our results suggest that the regulation of neuronal survival is one of the molecular mechanisms underlying the critical period for visual cortical neuroplasticity.

scholarly journals Rapid recovery from the effects of early monocular deprivation is enabled by temporary inactivation of the retinas

2016 ◽  
Vol 113 (49) ◽  
pp. 14139-14144 ◽  
Author(s):  
Ming-fai Fong ◽  
Donald E. Mitchell ◽  
Kevin R. Duffy ◽  
Mark F. Bear
Keyword(s):  
Visual Acuity ◽  
Visual Cortex ◽  
Binocular Vision ◽  
Visual Function ◽  
Visual Experience ◽  
Recovery Of Function ◽  
Monocular Deprivation ◽  
Synaptic Potentiation ◽  
Severe Impairment ◽  
Synaptic Changes

A half-century of research on the consequences of monocular deprivation (MD) in animals has revealed a great deal about the pathophysiology of amblyopia. MD initiates synaptic changes in the visual cortex that reduce acuity and binocular vision by causing neurons to lose responsiveness to the deprived eye. However, much less is known about how deprivation-induced synaptic modifications can be reversed to restore normal visual function. One theoretically motivated hypothesis is that a period of inactivity can reduce the threshold for synaptic potentiation such that subsequent visual experience promotes synaptic strengthening and increased responsiveness in the visual cortex. Here we have reduced this idea to practice in two species. In young mice, we show that the otherwise stable loss of cortical responsiveness caused by MD is reversed when binocular visual experience follows temporary anesthetic inactivation of the retinas. In 3-mo-old kittens, we show that a severe impairment of visual acuity is also fully reversed by binocular experience following treatment and, further, that prolonged retinal inactivation alone can erase anatomical consequences of MD. We conclude that temporary retinal inactivation represents a highly efficacious means to promote recovery of function.

scholarly journals Experience-dependent structural plasticity at pre- and postsynaptic sites of layer 2/3 cells in developing visual cortex

2019 ◽  
Author(s):  
Yujiao Jennifer Sun ◽  
J. Sebastian Espinosa ◽  
Mahmood S. Hoseini ◽  
Michael P. Stryker
Keyword(s):  
Visual Cortex ◽  
Primary Visual Cortex ◽  
Critical Period ◽  
Visual Experience ◽  
Visual Deprivation ◽  
Monocular Deprivation ◽  
Structural Basis ◽  
Dependent Plasticity ◽  
Anatomical Changes ◽  
Layer 2

AbstractThe developing brain can respond quickly to altered sensory experience by circuit reorganization. During a critical period in early life, neurons in the primary visual cortex rapidly lose responsiveness to an occluded eye and come to respond better to the open eye. While physiological and some of the molecular mechanisms of this process have been characterized, its structural basis, except for the well-known changes in the thalamocortical projection, remains obscure. To elucidate the relationship between synaptic remodeling and functional changes during this experience-dependent process, we used 2-photon microscopy to image synaptic structures of sparsely labeled layer 2/3 neurons in the binocular zone of mouse primary visual cortex. Anatomical changes at presynaptic and postsynaptic sites in mice undergoing monocular visual deprivation (MD) were compared to those in control mice with normal visual experience. We found that postsynaptic spines remodeled quickly in response to MD, with neurons more strongly dominated by the deprived eye losing more spines. These postsynaptic changes parallel changes in visual responses during MD and their recovery after restoration of binocular vision. In control animals with normal visual experience, the formation of presynaptic boutons increased during the critical period and then declined. MD affected bouton formation, but with a delay, blocking it after 3 days. These findings reveal intracortical anatomical changes in cellular layers of the cortex that can account for rapid activity-dependent plasticity.Significance statementThe operation of the cortex depends on the connections among its neurons. Taking advantage of molecular and genetic tools to label major proteins of the presynaptic and postsynaptic densities, we studied how connections of layer 2/3 excitatory neurons in mouse visual cortex were changed by monocular visual deprivation during the critical period, which causes amblyopia. The deprivation induced rapid remodeling of postsynaptic spines and impaired bouton formation. Structural measurement followed by calcium imaging demonstrated a strong correlation between changes in postsynaptic structures and functional responses in individual neurons after monocular deprivation. These findings suggest that anatomical changes at postsynaptic sites serve as a substrate for experience-dependent plasticity in the developing visual cortex.

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.

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