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Effects of whisker trimming on GABAA receptor binding in the barrel cortex of developing and adult rats

✍ Scribed by Fuchs, Jannon L.; Salazar, Eduardo


Publisher
John Wiley and Sons
Year
1998
Tongue
English
Weight
308 KB
Volume
395
Category
Article
ISSN
0021-9967

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✦ Synopsis


Both sensory deprivation and blockade of β₯-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, [ 3 H]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, [ 3 H]muscimol binding was 8.3% lower in deprived barrel rows than in adjacent nondeprived rows (P Ο½ 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 [ 3 H]MK-801 binding. Ten weeks after whiskers were allowed to regrow, the decrease in [ 3 H]muscimol binding was partly reversed (P Ο½ 0.002), leaving a 3.3% decrease (P Ο½ 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 Ο½ 0.001), indicating that the effect is not restricted to an early critical period. In rats trimmed for the first 10 postnatal days, [ 3 H]muscimol binding declined 2.3% (P Ο½ 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. J.


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