Hémart N, Daniel H, Jaillard D, Crépel F
URA CNRS 1121, Université Paris-Sud, Orsay, France.
Neurosci Res. 1994 Mar;19(2):213-21. doi: 10.1016/0168-0102(94)90145-7.
Long-term depression (LTD) of synaptic transmission at parallel fiber (PF)-Purkinje cell (PC) synapses occurs when these synapses are activated in conjunction with direct activation of voltage-gated calcium (Ca2+) channels of PCs. In the present study, we have used Aniracetam to test whether the expression of LTD at PF-PC synapses is due to a genuine modification of properties of alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionate (AMPA) receptors of these neurons. Whole-cell recordings of PF-mediated EPSCs were performed in thin slices taken from 16-22-day-old rats. In all tested cells, bath application of Aniracetam potentiated PF-mediated EPSCs and prolonged their decay without notably changing their rising phase. On the other hand, Aniracetam prevented the induction of LTD by a pairing protocol with Ca2+ spikes and, conversely, the nootropic compound had a larger potentiating effect on PF-mediated EPSCs during expression of LTD than normally, when this change in synaptic efficacy had been induced prior to Aniracetam application. These data strongly suggest that LTD involves a desensitization of postsynaptic AMPA receptors at PF-PC synapses, or, at least, a change in their functional characteristics.
当平行纤维（PF）-浦肯野细胞（PC）突触被激活并同时直接激活浦肯野细胞的电压门控钙（Ca2+）通道时，会发生突触传递的长期抑制（LTD）。在本研究中，我们使用茴拉西坦来测试PF-PC突触处LTD的表达是否源于这些神经元的α-氨基-3-羟基-5-甲基异恶唑-4-丙酸（AMPA）受体特性的真正改变。在取自16至22日龄大鼠的薄片中进行PF介导的兴奋性突触后电流（EPSC）的全细胞记录。在所有测试细胞中，浴灌茴拉西坦增强了PF介导的EPSC并延长了其衰减时间，而其上升相无明显变化。另一方面，茴拉西坦通过与Ca2+尖峰配对的方案阻止了LTD的诱导，相反，当在应用茴拉西坦之前已经诱导了突触效能的这种变化时，该促智化合物在LTD表达期间对PF介导的EPSC的增强作用比正常情况更大。这些数据强烈表明，LTD涉及PF-PC突触处突触后AMPA受体的脱敏，或者至少涉及其功能特性的改变。
