Metabotropic regulation of intrinsic excitability by synaptic activation of kainate receptors.
Metabotropic regulation of intrinsic excitability by synaptic activation of kainate receptors.
复制标题
通过海藻酸盐受体突触激活内在兴奋性的代谢性调节。
DOI：
10.1523/jneurosci.5356-03.2004
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发表时间：
2004-05-12
期刊：
影响因子：
--
通讯作者：
Wheal HV
中科院分区：
文献类型：
--
作者：
Melyan Z;Lancaster B;Wheal HV
内在神经元兴奋性的长期改变作为一种活动依赖性可塑性形式越来越受到重视。在这里，我们描述了这些变化的潜在突触启动机制，其中递质谷氨酸的释放作用于红藻氨酸受体以调节后尖峰慢后超极化（sAHP）。突触释放谷氨酸的这种作用被之前的红藻氨酸应用所阻断。此外，谷氨酸摄取的抑制增强了突触激活的效果。谷氨酸介导的红藻氨酸受体对 sAHP 电流 (IsAHP) 的抑制被 PKC 抑制剂 calphostin C 阻断，证实了代谢型信号级联的需要。这些数据描述了谷氨酸释放的新生理功能：代谢型红藻氨酸受体的激活，其直接控制锥体细胞的兴奋性，并可能导致长期的兴奋性变化。
Prolonged modification of intrinsic neuronal excitability is gaining prominence as an activity-dependent form of plasticity. Here we describe a potential synaptic initiation mechanism for these changes in which release of the transmitter glutamate acts on kainate receptors to regulate the postspike slow afterhyperpolarization (sAHP). This action of synaptically released glutamate was occluded by previous kainate application. Furthermore, inhibition of glutamate uptake enhanced the effects of synaptic activation. Glutamate-mediated kainate receptor inhibition of sAHP current (IsAHP) was blocked by the PKC inhibitor calphostin C, confirming the requirement for a metabotropic signaling cascade. These data describe a new physiological function for glutamate release: activation of metabotropic kainate receptors, which control directly the excitability of pyramidal cells and probably contribute to prolonged excitability changes.