通过在突触终端中增加的内部来抑制内细胞分裂
1Department of Neurobiology and Behavior, State University of New York, Stony Brook, 11794-5230.
Nature
|August 25, 1994
概括
细胞内 ([Ca2+]i) 的升高抑制了突触囊泡内细胞分解,这是神经递质循环的关键步骤. 这种依赖的反机制可以调节突触活动和抑郁.
科学领域:
- 神经科学是一个神经科学.
- 细胞生物学 细胞生物学
- 突触性可塑性 突触性可塑性
背景情况:
- 突触传播涉及囊泡的外细胞和内细胞.
- 通过内分细胞分裂来检索膜对于囊泡循环至关重要.
- 众所周知,外细胞分裂是依赖的.
研究的目的:
- 研究细胞内度 ([Ca2+]i) 在调节突触囊泡内细胞分裂中的作用.
- 为了确定是否会影响外细胞形成后膜回收的速度.
主要方法:
- 视网膜双极神经元的突触终端中的容量测量.
- 操纵细胞内水平以评估对内细胞分裂的影响.
主要成果:
- 内细胞分裂因[Ca2+]i升高而显著抑制.
- 膜检索的速度显示严重依赖于[Ca2+]i (希尔系数为4).
- 在[Ca2+]i >= 900 nM时,内细胞分裂完全被废除.
结论:
- 细胞内作为内细胞分裂的负反调节剂.
- 这种介导的反控制了神经递质分泌后的膜恢复.
- 该机制可能通过影响囊泡循环,导致活动依赖性突触抑制.
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