Chard P S, Jordán J, Marcuccilli C J, Miller R J, Leiden J M, Roos R P, Ghadge G D
Department of Pharmacological and Physiological Sciences, University of Chicago IL 60637, USA.
Proc Natl Acad Sci U S A. 1995 May 23;92(11):5144-8. doi: 10.1073/pnas.92.11.5144.
Distinct subpopulations of neurons in the brain contain one or more of the Ca(2+)-binding proteins calbindin D28k, calretinin, and parvalbumin. Although it has been shown that these high-affinity Ca(2+)-binding proteins can increase neuronal Ca2+ buffering capacity, it is not clear which aspects of neuronal physiology they normally regulate. To investigate this problem, we used a recently developed method for expressing calbindin D28k in the somatic and synaptic regions of cultured hippocampal pyramidal neurons. Ninety-six hours after infection with a replication-defective adenovirus containing the calbindin D28k gene, essentially all cultured hippocampal pyramidal neurons robustly expressed calbindin D28k. Our results demonstrate that while calbindin D28k does not alter evoked neurotransmitter release at excitatory pyramidal cell synapses, this protein has a profound effect on synaptic plasticity. In particular, we show that calbindin D28k expression suppresses posttetanic potentiation.
大脑中不同的神经元亚群含有一种或多种钙结合蛋白，如钙结合蛋白D28k、钙视网膜蛋白和小白蛋白。尽管已经表明这些高亲和力的钙结合蛋白可以增加神经元的钙缓冲能力，但它们通常调节神经元生理学的哪些方面尚不清楚。为了研究这个问题，我们使用了一种最近开发的方法，在培养的海马锥体神经元的体细胞和突触区域表达钙结合蛋白D28k。在用含有钙结合蛋白D28k基因的复制缺陷型腺病毒感染96小时后，基本上所有培养的海马锥体神经元都强烈表达钙结合蛋白D28k。我们的结果表明，虽然钙结合蛋白D28k不会改变兴奋性锥体细胞突触处诱发的神经递质释放，但这种蛋白对突触可塑性有深远影响。特别是，我们表明钙结合蛋白D28k的表达抑制强直后增强。
