Hartmann Jana, Konnerth Arthur
Institute of Neuroscience, Technische Universität München, Biedersteiner Str. 29, 80802, Munich, Germany.
Munich Cluster for Systems Neurology (SyNergy) and Center for Integrated Protein Sciences (CIPSM), Munich, Germany.
J Mol Med (Berl). 2015 Sep;93(9):983-9. doi: 10.1007/s00109-015-1298-7. Epub 2015 Jun 5.
The transient receptor potential (TRPC) proteins form non-selective cation channels that are activated downstream of Gq-phospholipase C-coupled receptors. TRPC3, one of the seven members of the TRPC subfamily, combines functions of an unspecific ion channel and a signal transducer. In the mammalian brain, the expression of TRPC3 is highest in cerebellar Purkinje cells, the principal neurons, and the sole output of the cerebellar cortex. In this review, we summarize findings identifying TRPC3 channels as integral components of glutamatergic metabotropic synaptic transmission. We give an overview of postsynaptic interaction partners and activation mechanisms of TRPC3 in central neurons. Finally, we address the deleterious consequences of distorted TRPC3 synaptic signaling for cerebellar function in different mouse models and present TRPC3 as an emerging candidate protein implicated in various forms of ataxia in humans.
瞬时受体电位（TRPC）蛋白形成非选择性阳离子通道，这些通道在与Gq - 磷脂酶C偶联的受体下游被激活。TRPC3是TRPC亚家族七个成员之一，兼具非特异性离子通道和信号转导器的功能。在哺乳动物大脑中，TRPC3在小脑浦肯野细胞（主要神经元，也是小脑皮质的唯一输出神经元）中表达最高。在这篇综述中，我们总结了将TRPC3通道鉴定为谷氨酸能代谢型突触传递不可或缺组成部分的研究发现。我们概述了TRPC3在中枢神经元中的突触后相互作用伙伴和激活机制。最后，我们阐述了在不同小鼠模型中TRPC3突触信号传导异常对小脑功能的有害影响，并提出TRPC3是与人类各种形式共济失调相关的一种新的候选蛋白。
