Effects of whisker trimming on GABA(A) receptor binding in the barrel cortex of developing and adult rats.
Both sensory deprivation and blockade of gamma-aminobutyric acid A (GABA(A)) receptors result in signs of cortical disinhibition. To investigate whether down-regulation of GABA(A) receptors could underlie effects of sensory deprivation, [3H]muscimol binding was assessed in rat whisker barrels after chronic whisker trimming. Vibrissae in row C or rows A,B,D, and E were trimmed during certain developmental periods. When whiskers were trimmed for the first 6 postnatal weeks, [3H]muscimol binding was 8.3% lower in deprived barrel rows than in adjacent nondeprived rows (P < 0.001). The effect may be somewhat selective for GABA(A) receptors because there was no evident change in N-methyl-D-aspartate (NMDA) receptors as indicated by [3H]MK-801 binding. Ten weeks after whiskers were allowed to regrow, the decrease in [3H]muscimol binding was partly reversed (P < 0.002), leaving a 3.3% decrease (P < 0.001). These declines in GABA(A) receptors could contribute to persisting electrophysiological signs of reduced inhibition in similarly deprived barrel neurons (Simons and Land [1987] Nature 326:694-697). A 6-week deprivation beginning in adulthood resulted in a 7.7% decrease (P < 0.001), indicating that the effect is not restricted to an early critical period. In rats trimmed for the first 10 postnatal days, [3H]muscimol binding declined 2.3% (P < 0.05), which is a small change compared with the magnitude of the developmental peak; thus, normal whisker input apparently is not required for the developmental increase in GABA(A) receptors. The present study suggests that sensory input can regulate cortical GABA(A) receptors in adulthood and during ontogeny. Down-regulation of cortical GABA(A) receptors may be a compensatory mechanism that serves to disinhibit the reduced sensory input.[1]References
- Effects of whisker trimming on GABA(A) receptor binding in the barrel cortex of developing and adult rats. Fuchs, J.L., Salazar, E. J. Comp. Neurol. (1998) [Pubmed]
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