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Climbing fiber-triggered metabotropic slow potentials enhance dendritic calcium transients and simple spike firing in cerebellar Purkinje cells

机译:攀爬的纤维触发的代谢慢电位增强小脑浦肯野细胞的树突状钙瞬变和简单的尖峰发射

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Cerebellar Purkinje cells (PCs) receive synaptic input from numerous parallel fibers (PFs) and from a single climbing fiber (CF). At both types of synapses, fast synaptic transmission is mediated by AMPA receptors, while at PIT synapses burst activity can additionally recruit metabotropic glutamate receptors (mGluRs) that mediate a slow depolarizing potential. Here, we show that mGluR-activated slow potentials can be evoked throughout the dendrite by CF-evoked complex spike tiring in the presence of an mGluR agonist. The CFtriggered mGluR potential was not only blocked by an mGluR antagonist but also when the CF-induced Ca2+ transient was blocked by an AMPA receptor antagonist, suggesting the possibility that the slow potential can be activated by the simultaneous occurrence of agonist binding at mGluRs and a CF-evoked Ca2+ transient. In turn, these CF-triggered slow mGluR potentials enhance the complex spike-associated calcium signals throughout the dendrite. Moreover, they provide a mechanism by which CFs can modulate the simple spike frequency of PCs. (c) 2007 Elsevier Inc. All rights reserved.
机译:小脑浦肯野细胞(PC)从众多平行纤维(PF)和单个攀爬纤维(CF)接收突触输入。在两种类型的突触中,快速的突触传递是由AMPA受体介导的,而在PIT突触中,爆发活性可以另外募集代谢型谷氨酸受体(mGluRs),介导缓慢的去极化潜能。在这里,我们显示了在存在mGluR激动剂的情况下,CF诱发的复杂尖峰疲劳可在整个枝晶中诱发mGluR激活的慢电位。 CF触发的mGluR电位不仅被mGluR拮抗剂阻断,而且当CF诱导的Ca2 +瞬变被AMPA受体拮抗剂阻断时,提示慢电位可能通过同时在mGluRs和受体上发生激动剂结合而被激活。 CF诱发的Ca2 +瞬变。反过来,这些CF触发的慢mGluR电位增强了整个枝晶中与尖峰相关的复杂钙信号。此外,它们提供了一种机制,CF可以通过该机制来调制PC的简单尖峰频率。 (c)2007 Elsevier Inc.保留所有权利。

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