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 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.

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

Functional aspects of plasticity in the visual system of adult cats after early monocular deprivation

1977 ◽  
Vol 278 (961) ◽  
pp. 411-424 ◽  
Keyword(s):  
Visual Cortex ◽  
Superior Colliculus ◽  
Lateral Geniculate Nucleus ◽  
Visual Stimuli ◽  
Monocular Deprivation ◽  
Early Deprivation ◽  
Optic Chiasma ◽  
Lateral Geniculate ◽  
Eyes Open ◽  
Y Cells

Responses to visual stimuli and to electrical stimulation of the optic chiasma were analysed in neurons of the lateral geniculate nucleus, visual cortex and superior colliculus in monocularly deprived cats with different post-deprivation periods. If the cats had both eyes open in their post-deprivation period (1 year) no recovery from the effects of early deprivation was found in the responses of neurones in all 3 visual structures. In cats with a post-deprivation reverse closure we found an increase in the proportion of Y-cells recorded in the early deprived layer of LGN when compared to the Y-cell proportion found in the same layers immediately after the deprived eye was opened. In neurons of the visual cortex and superior colliculus the functional abnormalities remained unaltered. The late closure of the non-deprived eye for up to 3 years did not effect neurons normally activated through that eye. Removal of the non-deprived eye unmasked connections of the deprived eye’s pathway onto neurons in the visual cortex and the superior colliculus. The neurons showed no specificity for the direction of movement or the orientation of visual stimuli. This recovery from deprivation was greater after enucleating the cats at the age of 6 months than at 18 months after birth. In the lateral geniculate nucleus of these cats the proportion of Y-cells in the recorded sample driven by the deprived eye had recovered to the value of normal cats. The difficulties in relating these physiological findings to results from morphological or behavioural studies are discussed.

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 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.

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.

Sign in / Sign up

Export Citation Format

Share Document