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细胞内钙离子对皮质GABA能神经元和小脑浦肯野细胞的峰电位编码调控方式不同。

Intracellular Ca2+ regulates spike encoding at cortical GABAergic neurons and cerebellar Purkinje cells differently.

作者信息

Qi Yulong, Huang Li, Ni Hong, Zhou Xin, Zhang Jing, Zhu Yan, Ge Ming, Guan Sudong, Wang Jin-Hui

机构信息

Department of Physiology, Bengbu Medical College, Bengbu Anhui 233000, China.

出版信息

Biochem Biophys Res Commun. 2009 Mar 27;381(1):129-33. doi: 10.1016/j.bbrc.2009.02.058. Epub 2009 Feb 23.

DOI:10.1016/j.bbrc.2009.02.058
PMID:19351606
Abstract

Spike encoding at GABAergic neurons plays an important role in maintaining the homeostasis of brain functions for well-organized behaviors. The rise of intracellular Ca2+ in GABAergic neurons causes synaptic plasticity. It is not clear how intracellular Ca2+ influences their spike encoding. We have investigated this issue at GFP-labeled GABAergic cortical neurons and cerebellar Purkinje cells by whole-cell recording in mouse brain slices. Our results show that an elevation of intracellular Ca2+ by infusing adenophostin-A lowers spike encoding at GABAergic cortical neurons and enhances encoding ability at cerebellar Purkinje cells. These differential effects of cytoplasmic Ca2+ on spike encoding are mechanistically associated with Ca2+-induced changes in the refractory periods and threshold potentials of sequential spikes, as well as with various expression ratios of CaM-KII to calcineurin in GABAergic cortical neurons and cerebellar Purkinje cells.

摘要

γ-氨基丁酸能神经元的动作电位编码在维持大脑功能稳态以实现有条不紊的行为方面起着重要作用。γ-氨基丁酸能神经元内细胞内Ca2+的升高会导致突触可塑性。目前尚不清楚细胞内Ca2+如何影响其动作电位编码。我们通过在小鼠脑片上进行全细胞记录,对绿色荧光蛋白标记的γ-氨基丁酸能皮质神经元和小脑浦肯野细胞进行了研究。我们的结果表明,通过注入腺嘌呤核苷酸A使细胞内Ca2+升高会降低γ-氨基丁酸能皮质神经元的动作电位编码,并增强小脑浦肯野细胞的编码能力。细胞质Ca2+对动作电位编码的这些不同影响在机制上与Ca2+诱导的连续动作电位不应期和阈电位变化有关,也与γ-氨基丁酸能皮质神经元和小脑浦肯野细胞中CaM-KII与钙调神经磷酸酶的各种表达比率有关。

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