抑制性突触后电位
γ-氨基丁酸受体
小脑
蛋白质亚单位
神经科学
生物
受体
突触后电流
NMDA受体
化学
神经传递
生物物理学
兴奋性突触后电位
生物化学
基因
作者
Stefano Vicini,Carolyn Ferguson,Kate Prybylowski,Jason E. Kralic,A. Leslie Morrow,Gregg E. Homanics
标识
DOI:10.1523/jneurosci.21-09-03009.2001
摘要
Developmental changes in miniature IPSC (mIPSC) kinetics have been demonstrated previously in cerebellar neurons in rodents. We report that these kinetic changes in mice are determined primarily by developmental changes in GABA A receptor subunit expression. mIPSCs were studied by whole-cell recordings in cerebellar slices, prepared from postnatal day 11 (P11) and P35 mice. Similar to reports in granule neurons, wild-type cerebellar stellate neuron mIPSCs at P11 had slow decay kinetics, whereas P35 mIPSCs decayed five times faster. When mIPSCs in cerebellar stellate neurons were compared between wild-type (+/+) and GABA A receptor α1 subunit-deficient (−/−) littermates at P35, we observed dramatically slower mIPSC decay rates in −/− animals. We took advantage of the greater potency of imidazopyridines for GABA current potentiation with α1 subunit-containing receptors to characterize the relative contribution of α1 subunits in native receptors on inhibitory synapses of cerebellar granule neurons. Zolpidem-induced prolongation of mIPSC decay was variable among distinct cells, but it increased during development in wild-type mice. Similarly, Zolpidem prolongation of mIPSC decay rate was significantly greater in adult +/+ mice than in knock-outs. We propose that an increased α1 subunit assembly in postsynaptic receptors of cerebellar inhibitory synapses is responsible for the fast inhibitory synaptic currents that are normally observed during postnatal development.
科研通智能强力驱动
Strongly Powered by AbleSci AI