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突触足蛋白调节培养海马神经元树突棘中钙库的释放。

Synaptopodin regulates release of calcium from stores in dendritic spines of cultured hippocampal neurons.

机构信息

Department of Neurobiology, The Weizmann Institute, 76100 Rehovot, Israel.

出版信息

J Physiol. 2011 Dec 15;589(Pt 24):5987-95. doi: 10.1113/jphysiol.2011.217315. Epub 2011 Oct 24.

Abstract

The presence of calcium stores and their function in dendritic spines is still unsettled. We have now studied the kinetics of calcium released inside dendritic spines of cultured rat hippocampal neurons by flash photolysis of caged calcium. Photolysis of calcium produced a fast rise in Ca(2+), followed by a variable decay. We were able to correlate the decay of elevated Ca(2+) with the presence of synaptopodin (SP), an actin-binding protein, in the spines; spines containing SP generated the same initial Ca(2+) transient, but their decay time was significantly slower and more complex than that of SP-negative ones. The altered decay kinetics of the flash-elevated Ca(2+) transient was blocked by thapsigargin or cyclopiazonic acid (CPA), indicating that this kinetic change is due to compartmentalized release of calcium from intracellular stores. Thus, SP plays a pivotal role in the calcium store-associated ability of spines to locally tune calcium kinetics.

摘要

钙储存的存在及其在树突棘中的功能仍未确定。我们现在通过光解笼状钙研究了培养的大鼠海马神经元树突棘内释放的钙的动力学。钙的光解产生了 Ca(2+) 的快速上升,随后是可变的衰减。我们能够将升高的 Ca(2+) 的衰减与树突棘中的肌动蛋白结合蛋白 synaptopodin (SP) 的存在相关联;含有 SP 的棘突产生相同的初始 Ca(2+) 瞬变,但它们的衰减时间明显慢于且比 SP 阴性棘突更复杂。钙瞬变的这种衰减动力学的改变被 thapsigargin 或环匹阿尼酸 (CPA) 阻断,表明这种动力学变化是由于细胞内储存的钙从隔室中释放。因此,SP 在与钙储存相关的棘突局部调节钙动力学的能力中发挥着关键作用。

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