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.

Functional postnatal development of the rat primary visual cortex and the role of visual experience: Dark rearing and monocular deprivation

1994 ◽  
Vol 34 (6) ◽  
pp. 709-720 ◽  
Author(s):  
Michela Fagiolini ◽  
Tommaso Pizzorusso ◽  
Nicoletta Berardi ◽  
Luciano Domenici ◽  
Lamberto Maffei
Keyword(s):  
Visual Cortex ◽  
Postnatal Development ◽  
Primary Visual Cortex ◽  
Visual Experience ◽  
Monocular Deprivation ◽  
Dark Rearing

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 Correction of amblyopia in cats and mice after the critical period

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Ming-fai Fong ◽  
Kevin R Duffy ◽  
Madison P Leet ◽  
Christian T Candler ◽  
Mark F Bear
Keyword(s):  
Visual Cortex ◽  
Visual Impairment ◽  
Primary Visual Cortex ◽  
Critical Period ◽  
Alternative Explanation ◽  
Monocular Deprivation ◽  
Interocular Suppression ◽  
Fellow Eye ◽  
Clinical Observations

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.

scholarly journals Correction of amblyopia in cats and mice after the critical period

2021 ◽  
Author(s):  
Ming-fai Fong ◽  
Kevin R. Duffy ◽  
Madison P. Leet ◽  
Christian T. Candler ◽  
Mark F. Bear
Keyword(s):  
Visual Cortex ◽  
Visual Impairment ◽  
Primary Visual Cortex ◽  
Critical Period ◽  
Alternative Explanation ◽  
Monocular Deprivation ◽  
Interocular Suppression ◽  
Fellow Eye ◽  
Clinical Observations

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 by relieving interocular suppression in primary visual cortex. However, an alternative explanation is that elimination of activity in the fellow eye establishes conditions in visual cortex that enable the weak connections from the amblyopic eye to gain strength. Here we show 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.

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.

scholarly journals Elastic Net Model of Ocular Dominance: Overall Stripe Pattern and Monocular Deprivation

1994 ◽  
Vol 6 (4) ◽  
pp. 615-621 ◽  
Author(s):  
Geoffrey J. Goodhill ◽  
David J. Willshaw
Keyword(s):  
Visual Cortex ◽  
Lateral Geniculate Nucleus ◽  
Primary Visual Cortex ◽  
Ocular Dominance ◽  
Monocular Deprivation ◽  
Elastic Net ◽  
Global Order ◽  
Stripe Pattern ◽  
Lateral Geniculate ◽  
Stripe Width

The elastic net (Durbin and Willshaw 1987) can account for the development of both topography and ocular dominance in the mapping from the lateral geniculate nucleus to primary visual cortex (Goodhill and Willshaw 1990). Here it is further shown for this model that (1) the overall pattern of stripes produced is strongly influenced by the shape of the cortex: in particular, stripes with a global order similar to that seen biologically can be produced under appropriate conditions, and (2) the observed changes in stripe width associated with monocular deprivation are reproduced in the model.

scholarly journals Input-specific maturation of NMDAR-mediated transmission onto parvalbumin-expressing interneurons in layers 2/3 of the visual cortex

2018 ◽  
Vol 120 (6) ◽  
pp. 3063-3076 ◽  
Author(s):  
Camilo Ferrer ◽  
Helen Hsieh ◽  
Lonnie P. Wollmuth
Keyword(s):  
Visual Cortex ◽  
Critical Period ◽  
Pyramidal Neurons ◽  
Temporal Integration ◽  
Developmental Changes ◽  
Evoked Responses ◽  
Developmentally Regulated ◽  
Low Frequencies ◽  
Aspartate Receptor ◽  
Synaptic Responses

Parvalbumin-expressing (PV) GABAergic interneurons regulate local circuit dynamics. In terms of the excitation driving PV interneuron activity, the N-methyl-d-aspartate receptor (NMDAR)-mediated component onto PV interneurons tends to be smaller than that onto pyramidal neurons but makes a significant contribution to their physiology and development. In the visual cortex, PV interneurons mature during the critical period. We hypothesize that during the critical period, the NMDAR-mediated signaling and functional properties of glutamatergic synapses onto PV interneurons are developmentally regulated. We therefore compared the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR)- and NMDAR-mediated synaptic responses before (postnatal days 15–20, P15–P20), during (P25–P40), and after (P50–P60) the visual critical period. AMPAR miniature excitatory postsynaptic currents (mEPSCs) showed a developmental decrease in frequency, whereas NMDAR mEPSCs were absent or showed extremely low frequencies throughout development. For evoked responses, we consistently saw a NMDAR-mediated component, suggesting pre- or postsynaptic differences between evoked and spontaneous neurotransmission. Evoked responses showed input-specific developmental changes. For intralaminar inputs, the NMDAR-mediated component significantly decreased with development. This resulted in adult intralaminar inputs almost exclusively mediated by AMPARs, suited for the computation of synaptic inputs with precise timing, and likely having NMDAR-independent forms of plasticity. In contrast, interlaminar inputs maintained a stable NMDAR-mediated component throughout development but had a shift in the AMPAR paired-pulse ratio from depression to facilitation. Adult interlaminar inputs with facilitating AMPAR responses and a substantial NMDAR component would favor temporal integration of synaptic responses and could be modulated by NMDAR-dependent forms of plasticity. NEW & NOTEWORTHY We show for the first time input-specific developmental changes in the N-methyl-d-aspartate receptor component and short-term plasticity of the excitatory drive onto layers 2/3 parvalbumin-expressing (PV) interneurons in the visual cortex during the critical period. These developmental changes would lead to functionally distinct adult intralaminar and interlaminar glutamatergic inputs that would engage PV interneuron-mediated inhibition differently.

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