Coincidence detection and changes of synaptic efficacy in spiny stellate neurons in vat barrel cortex
Coincidence detection and changes of synaptic efficacy in spiny stellate neurons in vat barrel cortex
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DOI：
10.1038/16026
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发表时间：
1999-12-01
影响因子：
25
通讯作者：
Sakmann, B
中科院分区：
文献类型：
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作者：
Egger, V;Feldmeyer, D;Sakmann, B
成对的全细胞电压记录从突触连接的多刺星状神经元在第4层的桶场在年轻（P14）大鼠体感皮层。当突触后动作电位（AP）遵循每5个突触前AP在10或20 Hz的列车不到25 ms，随后的单一EPSP幅度持续降低。长期抑郁症（LTD）的诱导依赖于II组代谢型谷氨酸受体的激活，但不依赖于NMDA或AMPA受体。通过细胞内加载快效（BAPTA）或慢效（EGTA）Ca2+缓冲剂，减少突触后细胞内钙（[Ca2+]（i））增加，阻断突触抑制。EPSP故障分析表明，通过降低释放概率来调解LTD。我们提出了一种机制，通过该机制，同时活动导致突触连接的神经元之间的突触效能的长期降低。
Paired whole-cell voltage recordings were made from synaptically connected spiny stellate neurons in layer 4 of the barrel field in young (P14) rat somatosensory cortex. When postsynaptic action potentials (APs) followed each of 5 presynaptic APs in a 10- or 20-Hz train by less than 25 ms, subsequent unitary EPSP amplitudes were persistently reduced. Induction of long-term depression (LTD) depended on activation of group II metabotropic glutamate receptors, but not on NMDA or AMPA receptors. Reducing postsynaptic increases in intracellular calcium ([Ca2+](i)) by intracellular loading with a fast- (BAPTA) or a slow- (EGTA) acting Ca2+ buffer blocked synaptic depression. Analysis of EPSP failures suggested mediation of LTD by a reduction in release probability. We propose a mechanism by which coincident activity results in long-lasting reduction of synaptic efficacy between synaptically connected neurons.