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Structure. 2008 Oct 8;16(10):1455-67. doi: 10.1016/j.str.2008.07.010.
2
Phosphorylation of Homer3 by calcium/calmodulin-dependent kinase II regulates a coupling state of its target molecules in Purkinje cells.钙/钙调蛋白依赖性激酶II对Homer3的磷酸化作用调节浦肯野细胞中其靶分子的偶联状态。
J Neurosci. 2008 May 14;28(20):5369-82. doi: 10.1523/JNEUROSCI.4738-07.2008.
3
Crystal structure of the CaV2 IQ domain in complex with Ca2+/calmodulin: high-resolution mechanistic implications for channel regulation by Ca2+.与Ca2+/钙调蛋白结合的CaV2 IQ结构域的晶体结构：Ca2+对通道调节的高分辨率机制研究
Structure. 2008 Apr;16(4):607-20. doi: 10.1016/j.str.2008.01.011.
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The leaner P/Q-type calcium channel mutation renders cerebellar Purkinje neurons hyper-excitable and eliminates Ca2+-Na+ spike bursts.更瘦的P/Q型钙通道突变使小脑浦肯野神经元过度兴奋，并消除Ca2+-Na+ 尖峰爆发。
Eur J Neurosci. 2008 Jan;27(1):93-103. doi: 10.1111/j.1460-9568.2007.05998.x. Epub 2007 Dec 17.
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Novel CaV2.1 clone replicates many properties of Purkinje cell CaV2.1 current.新型CaV2.1克隆体复制了浦肯野细胞CaV2.1电流的许多特性。
Eur J Neurosci. 2007 Nov;26(10):2950-61. doi: 10.1111/j.1460-9568.2007.05912.x.
6
Long-term depression of mGluR1 signaling.代谢型谷氨酸受体1信号通路的长期抑制
Neuron. 2007 Jul 19;55(2):277-87. doi: 10.1016/j.neuron.2007.06.035.
7
Differential regulation of endogenous N- and P/Q-type Ca2+ channel inactivation by Ca2+/calmodulin impacts on their ability to support exocytosis in chromaffin cells.Ca2+/钙调蛋白对内源性N型和P/Q型Ca2+通道失活的差异调节影响其在嗜铬细胞中支持胞吐作用的能力。
J Neurosci. 2007 May 9;27(19):5236-48. doi: 10.1523/JNEUROSCI.3545-06.2007.
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Elementary mechanisms producing facilitation of Cav2.1 (P/Q-type) channels.产生Cav2.1（P/Q型）通道易化作用的基本机制。
J Gen Physiol. 2007 May;129(5):385-401. doi: 10.1085/jgp.200709749. Epub 2007 Apr 16.
9
Spino-dendritic cross-talk in rodent Purkinje neurons mediated by endogenous Ca2+-binding proteins.内源性钙结合蛋白介导的啮齿动物浦肯野神经元中的脊髓-树突串扰
J Physiol. 2007 Jun 1;581(Pt 2):619-29. doi: 10.1113/jphysiol.2007.127860. Epub 2007 Mar 8.
10
Differences in locomotor behavior revealed in mice deficient for the calcium-binding proteins parvalbumin, calbindin D-28k or both.在缺乏钙结合蛋白小白蛋白、钙结合蛋白D-28k或两者的小鼠中所揭示的运动行为差异。
Behav Brain Res. 2007 Mar 28;178(2):250-61. doi: 10.1016/j.bbr.2007.01.002. Epub 2007 Jan 5.

缺乏钙结合蛋白 Parvalbumin 和钙结合蛋白 D-28k 的小脑浦肯野神经元中 Cav2.1 Ca2+ 通道的代偿性调节。

Compensatory regulation of Cav2.1 Ca2+ channels in cerebellar Purkinje neurons lacking parvalbumin and calbindin D-28k.

机构信息

Department of Molecular Physiology and Biophysics, University of Iowa, 51 Newton Road, Iowa City, IA 52242, USA.

出版信息

J Neurophysiol. 2010 Jan;103(1):371-81. doi: 10.1152/jn.00635.2009. Epub 2009 Nov 11.

DOI:10.1152/jn.00635.2009
PMID:19906882
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2807225/
Abstract

Ca(v)2.1 channels regulate Ca(2+) signaling and excitability of cerebellar Purkinje neurons. These channels undergo a dual feedback regulation by incoming Ca(2+) ions, Ca(2+)-dependent facilitation and inactivation. Endogenous Ca(2+)-buffering proteins, such as parvalbumin (PV) and calbindin D-28k (CB), are highly expressed in Purkinje neurons and therefore may influence Ca(v)2.1 regulation by Ca(2+). To test this, we compared Ca(v)2.1 properties in dissociated Purkinje neurons from wild-type (WT) mice and those lacking both PV and CB (PV/CB(-/-)). Unexpectedly, P-type currents in WT and PV/CB(-/-) neurons differed in a way that was inconsistent with a role of PV and CB in acute modulation of Ca(2+) feedback to Ca(v)2.1. Ca(v)2.1 currents in PV/CB(-/-) neurons exhibited increased voltage-dependent inactivation, which could be traced to decreased expression of the auxiliary Ca(v)beta(2a) subunit compared with WT neurons. Although Ca(v)2.1 channels are required for normal pacemaking of Purkinje neurons, spontaneous action potentials were not different in WT and PV/CB(-/-) neurons. Increased inactivation due to molecular switching of Ca(v)2.1 beta-subunits may preserve normal activity-dependent Ca(2+) signals in the absence of Ca(2+)-buffering proteins in PV/CB(-/-) Purkinje neurons.

摘要

钙通道 2.1（Ca(v)2.1）调控小脑浦肯野神经元的钙离子信号和兴奋。这些通道通过钙离子内流进行双重反馈调节，包括钙离子依赖性易化和失活。内源性钙缓冲蛋白，如钙结合蛋白 D-28k（CB）和 Parvalbumin（PV）在浦肯野神经元中高度表达，因此可能影响 Ca(v)2.1 的调节。为了验证这一点，我们比较了来自野生型（WT）和缺乏 PV 和 CB（PV/CB(-/-)）的浦肯野神经元中的 Ca(v)2.1 特性。出乎意料的是，WT 和 PV/CB(-/-)神经元中的 P 型电流的差异方式与 PV 和 CB 对 Ca(v)2.1 的钙离子反馈的急性调节作用不一致。PV/CB(-/-)神经元中的 Ca(v)2.1 电流表现出增加的电压依赖性失活，这可以追溯到与 WT 神经元相比，辅助 Ca(v)beta(2a)亚基的表达减少。尽管 Ca(v)2.1 通道是浦肯野神经元正常起搏所必需的，但 WT 和 PV/CB(-/-)神经元中的自发性动作电位没有差异。由于 Ca(v)2.1 beta 亚基的分子开关，失活增加可能在缺乏 PV/CB(-/-)浦肯野神经元中的钙缓冲蛋白的情况下，维持正常的活动依赖性钙信号。