Genetic and epigenetic regulation of NMDA receptor expression in the rat visual cortex

The susceptibility of cortical networks to use‐dependent modifications declines with age (critical period) and this decline of neuronal plasticity during development is paralleled by the shortening of NMDA receptor EPSCs. We showed previously in the somatosensory cortex that the shortening of NMDA r...

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Veröffentlicht in:The European journal of neuroscience 1999-12, Vol.11 (12), p.4320-4326
Hauptverfasser: Nase, Gabriele, Weishaupt, Jochen, Stern, Peter, Singer, Wolf, Monyer, Hannah
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Sprache:eng
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Zusammenfassung:The susceptibility of cortical networks to use‐dependent modifications declines with age (critical period) and this decline of neuronal plasticity during development is paralleled by the shortening of NMDA receptor EPSCs. We showed previously in the somatosensory cortex that the shortening of NMDA receptor kinetics correlates with a developmentally‐regulated increase in the NR2A subunit expression. Here we examine whether this developmental regulation of NR2A expression is related to the duration of critical periods and whether it is influenced by experience. Functional NMDA receptors and their molecular characteristics are studied in identified layer IV neurons of rat visual cortex. In this structure the time course of the critical period differs from that in the somatosensory cortex and can be changed by sensory deprivation, thus permitting examination of correlations between the time course of receptor expression and the duration of the critical period. We find that the developmental expression of the NR2A subunit is delayed compared with the somatosensory cortex, in agreement with the prolonged critical period in the visual cortex. Moreover, sensory deprivation further delays the developmental change in the NMDA receptor subunit composition, demonstrating the activity dependence of this process and strengthening the correlation between changes in subunit composition and the time course of the critical period.
ISSN:0953-816X
1460-9568
DOI:10.1046/j.1460-9568.1999.00859.x