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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Mechanisms of induction and expression of long-term depression at GABAergic synapses in the neonatal rat hippocampus.
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Mechanisms of induction and expression of long-term depression at GABAergic synapses in the neonatal rat hippocampus.

机译:新生大鼠海马中GABA能突触的诱导和长期抑制的表达机制。

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摘要

Synaptic plasticity at excitatory glutamatergic synapses is believed to be instrumental in the maturation of neuronal networks. Using whole-cell patch-clamp recordings, we have studied the mechanisms of induction and expression of long-term depression at excitatory GABAergic synapses in the neonatal rat hippocampus (LTD(GABA-A)). We report that the induction of LTD(GABA-A) requires a GABA(A) receptor-mediated membrane depolarization, which is necessary to remove the Mg(2+) block from postsynaptic NMDA receptors. LTD(GABA-A) is associated with an increase in the coefficient of variation of evoked GABA(A) receptor-mediated synaptic currents and a decrease in the frequency, but not amplitude, of Sr(2+)-induced asynchronous GABA(A) quantal events. We conclude that LTD(GABA-A) induction requires the activation of both GABA(A) and NMDA postsynaptic receptors and that its expression is likely presynaptic.
机译:兴奋性谷氨酸能突触的突触可塑性被认为在神经元网络的成熟中起重要作用。使用全细胞膜片钳录音,我们研究了新生大鼠海马兴奋性GABA能突触中的长期抑制的诱导和表达机制(LTD(GABA-A))。我们报告,LTD(GABA-A)的诱导需要一个GABA(A)受体介导的膜去极化,这对于从突触后NMDA受体去除Mg(2+)块是必要的。 LTD(GABA-A)与诱发的GABA(A)受体介导的突触电流的变异系数增加以及Sr(2+)诱导的异步GABA(A)的频率而非振幅降低相关)数量事件。我们得出结论,LTD(GABA-A)诱导需要激活GABA(A)和NMDA突触后受体,并且其表达可能在突触前。

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