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依赖三磷酸肌醇的钙诱导钙释放介导神经元中的双向钙波:对突触可塑性的功能影响

IP3-dependent calcium-induced calcium release mediates bidirectional calcium waves in neurones: functional implications for synaptic plasticity.

作者信息

Barbara J-G

机构信息

Laboratoire de Neurobiologie des Processus Adaptatifs, UMR CNRS 7102, 7 Quai Saint Bernard, Case 8, Paris, France.

出版信息

Biochim Biophys Acta. 2002 Nov 4;1600(1-2):12-8. doi: 10.1016/s1570-9639(02)00439-9.

Abstract

IP(3)-dependent calcium-induced calcium release (ICICR) is a general mechanism of calcium release that occurs in pyramidal neurones of hippocampus, the neocortex and in Purkinje cells of the cerebellar cortex. When ICICR is initiated synaptically in dendrites of neurones from brain slices, calcium waves can propagate bidirectionally to the soma and distal dendrites. ICICR relies on the coincidence of a calcium influx triggered by the backpropagation of action potentials and the activation of cholinergic, serotoninergic or glutamatergic metabotropic receptors. The involvement of IP(3) receptors (IP(3)R) in ICICR is clearly established. In contrast, ryanodine receptors (RyR) do not seem necessary for the triggering and propagation of calcium waves, but ICICR depends on calcium stores sensitive to ryanodine. Thus, the role of RyR remains to be established. ICICR provides a mechanism for global calcium signalling in neurones that may be involved in the reinforcement of Hebbian plasticity, heterosynaptic plasticity and cell death.

摘要

依赖三磷酸肌醇(IP(3))的钙诱导钙释放(ICICR)是一种普遍的钙释放机制,发生于海马体的锥体神经元、新皮层以及小脑皮层的浦肯野细胞中。当在脑片神经元的树突中通过突触引发ICICR时,钙波可双向传播至胞体和远端树突。ICICR依赖于动作电位反向传播引发的钙内流与胆碱能、5-羟色胺能或谷氨酸能代谢型受体激活的同时发生。IP(3)受体(IP(3)R)参与ICICR已得到明确证实。相比之下,兰尼碱受体(RyR)似乎并非钙波触发和传播所必需,但ICICR依赖于对兰尼碱敏感的钙库。因此,RyR的作用仍有待确定。ICICR为神经元中的全局钙信号传导提供了一种机制,这可能与赫布可塑性、异突触可塑性的增强以及细胞死亡有关。

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