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钙结合蛋白小白蛋白在短期突触可塑性中的作用。

Role of the calcium-binding protein parvalbumin in short-term synaptic plasticity.

作者信息

Caillard O, Moreno H, Schwaller B, Llano I, Celio M R, Marty A

机构信息

Max-Planck-Institute for Biophysical Chemistry, D37 077 Göttingen, Germany.

出版信息

Proc Natl Acad Sci U S A. 2000 Nov 21;97(24):13372-7. doi: 10.1073/pnas.230362997.

DOI:10.1073/pnas.230362997
PMID:11069288
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC27231/
Abstract

GABAergic (GABA = gamma-aminobutyric acid) neurons from different brain regions contain high levels of parvalbumin, both in their soma and in their neurites. Parvalbumin is a slow Ca(2+) buffer that may affect the amplitude and time course of intracellular Ca(2+) transients in terminals after an action potential, and hence may regulate short-term synaptic plasticity. To test this possibility, we have applied paired-pulse stimulations (with 30- to 300-ms intervals) at GABAergic synapses between interneurons and Purkinje cells, both in wild-type (PV+/+) mice and in parvalbumin knockout (PV-/-) mice. We observed paired-pulse depression in PV+/+ mice, but paired-pulse facilitation in PV-/- mice. In paired recordings of connected interneuron-Purkinje cells, dialysis of the presynaptic interneuron with the slow Ca(2+) buffer EGTA (1 mM) rescues paired-pulse depression in PV-/- mice. These data show that parvalbumin potently modulates short-term synaptic plasticity.

摘要

来自不同脑区的γ-氨基丁酸能(GABA = γ-氨基丁酸)神经元,其胞体和神经突中都含有高水平的小白蛋白。小白蛋白是一种缓慢的Ca²⁺缓冲蛋白,可能会影响动作电位后终末内细胞内Ca²⁺瞬变的幅度和时程,因此可能调节短期突触可塑性。为了验证这种可能性,我们在野生型(PV+/+)小鼠和小白蛋白基因敲除(PV-/-)小鼠的中间神经元与浦肯野细胞之间的γ-氨基丁酸能突触处施加了配对脉冲刺激(间隔30至300毫秒)。我们在PV+/+小鼠中观察到配对脉冲抑制,但在PV-/-小鼠中观察到配对脉冲易化。在相连的中间神经元-浦肯野细胞的配对记录中,用缓慢的Ca²⁺缓冲剂乙二醇双四乙酸(EGTA,1 mM)对突触前中间神经元进行透析可挽救PV-/-小鼠中的配对脉冲抑制。这些数据表明,小白蛋白有力地调节短期突触可塑性。

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