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Two Ca(2+)-dependent steps controlling synaptic vesicle fusion and replenishment at the cerebellar basket cell terminal.

机译:两个Ca(2+)依赖步骤控制小脑篮细胞末端的突触囊泡融合和补充。

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摘要

Cerebellar basket cells inhibit postsynaptic Purkinje cells in a rapid and precise manner. To investigate the mechanisms of transmitter release underlying this rapid inhibition, Ca(2+) uncaging was employed to measure the intracellular Ca(2+) dependence of transmitter release and the kinetics of synaptic vesicle pool transitions in immature basket cell synapses at room temperature. Vesicle release properties distinct from those previously observed at excitatory synapses were seen, including a relatively high intracellular Ca(2+) sensitivity of vesicle fusion, rapid vesicle pool mobilization with few reluctant vesicles, and vesicle replenishment driven by unusually high Ca(2+) levels from both local and residual Ca(2+) sources during action potential trains. These results suggest that inhibitory basket cell synapses are optimized for rapid and precise temporal and spatial Ca(2+) coordination of synaptic vesicle fusion and replenishment, which may contribute to the unique physiology of inhibitory synaptic transmission, including phasic release during action potential trains and tonic release by residual intracellular Ca(2+).
机译:小脑篮细胞以快速而精确的方式抑制突触后浦肯野细胞。为了研究这种快速抑制作用下递质释放的机制,采用Ca(2+)解笼法来测量递质释放的细胞内Ca(2+)依赖性以及室温下未成熟篮子细胞突触中突触囊泡池转变的动力学。囊泡释放特性不同于先前在兴奋性突触中观察到的释放特性,包括相对较高的胞内Ca(2+)囊泡融合敏感性,快速囊泡池动员,很少有不希望的囊泡,以及由异常高的Ca(2+)驱动的囊泡补给动作电位训练过程中从本地和残留Ca(2+)来源的水平。这些结果表明抑制篮细胞突触优化突触小泡融合和补充的快速和精确的时间和空间Ca(2+)协调,这可能有助于抑制突触传递的独特生理,包括在动作电位训练和释放期间的阶段性释放。残余细胞内Ca(2+)释放补品。

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