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Strontium as a substitute for calcium in the process of transmitter release at the neuromuscular junction.在神经肌肉接头处递质释放过程中锶作为钙的替代物。
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Long-term potentiation of GABAergic synaptic transmission in neonatal rat hippocampus.新生大鼠海马体中γ-氨基丁酸能突触传递的长期增强作用
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Sr2+ supports depolarization-induced suppression of inhibition and provides new evidence for a presynaptic expression mechanism in rat hippocampal slices.Sr2+ 支持去极化诱导的抑制作用抑制，并为大鼠海马切片中的突触前表达机制提供了新证据。
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新生大鼠海马体中GABA能突触处长期抑制的诱导和表达机制。

Mechanisms of induction and expression of long-term depression at GABAergic synapses in the neonatal rat hippocampus.

作者信息

Caillard O, Ben-Ari Y, Gaïarsa J L

机构信息

Institut de Neurobiologie de la Mediterranée (INMED), Institut National de la Santé et de la Recherche Médicale U29, B.P. 13, 13273 Marseille Cedex 09, France.

出版信息

J Neurosci. 1999 Sep 1;19(17):7568-77. doi: 10.1523/JNEUROSCI.19-17-07568.1999.

DOI:10.1523/JNEUROSCI.19-17-07568.1999
PMID:10460263
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6782510/
Abstract

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.

摘要

兴奋性谷氨酸能突触的突触可塑性被认为对神经网络的成熟至关重要。我们使用全细胞膜片钳记录技术，研究了新生大鼠海马体中兴奋性GABA能突触处长期抑制（LTD(GABA-A)）的诱导和表达机制。我们报告称，LTD(GABA-A)的诱导需要GABA(A)受体介导的膜去极化，这对于从突触后NMDA受体上去除Mg(2+)阻滞是必要的。LTD(GABA-A)与诱发的GABA(A)受体介导的突触电流变异系数增加以及Sr(2+)诱导的异步GABA(A)量子事件频率降低（而非幅度降低）相关。我们得出结论，LTD(GABA-A)的诱导需要GABA(A)和NMDA突触后受体的激活，并且其表达可能是突触前的。