Calcium signaling and synaptic modulation: Regulation of endocannabinoid-mediated synaptic modulation by calcium
Calcium signaling and synaptic modulation: Regulation of endocannabinoid-mediated synaptic modulation by calcium
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DOI：
10.1016/j.ceca.2005.06.014
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发表时间：
2005-09-01
期刊：
影响因子：
4
通讯作者：
Kano, M
中科院分区：
文献类型：
--
作者：
Ohno-Shosaku, T;Hashimotodani, Y;Kano, M
突触后钙离子（Ca2+）信号通过多种机制影响突触传递。其中一些机制涉及逆向信使，这些信使以钙离子依赖的方式从突触后神经元释放，并通过激活突触前受体来调节递质释放。近期研究揭示了内源性大麻素在突触传递逆向调节中的关键作用。内源性大麻素的释放可由突触后钙离子单独升高引发，也可由突触后与G(q/11)偶联的受体激活引发，无论是否伴有钙离子升高。前一种途径不依赖磷脂酶Cβ（PLCβ），需要钙离子大幅升高至微摩尔浓度范围。后一种途径需要PLCβ，且适度升高钙离子至亚微摩尔浓度范围可促进该过程。这种促进作用源于受体驱动的PLCβ激活对钙离子的依赖性。释放的内源性大麻素随后激活突触前1型大麻素受体（CB1），并抑制突触前末梢的递质释放。CB1受体和与G(q/11)偶联的受体在大脑中广泛分布。因此，内源性大麻素介导的逆向调节可能是大脑中一种重要且普遍存在的机制，通过这一机制，包括与G(q/11)偶联的受体激活和钙离子升高在内的突触后事件能够逆向影响突触前功能。（C）2005爱思唯尔有限公司。保留所有权利。
Postsynaptic Ca2+ signal influences synaptic transmission through multiple mechanisms. Some of them involve retrograde messengers that are released from postsynaptic neurons in a Ca2+-dependent manner and modulate transmitter release through activation of presynaptic receptors. Recent studies have revealed essential roles of endocannabinoids in retrograde modulation of synaptic transmission. Endocannabinoid release is induced by either postsynaptic Ca2+ elevation alone or activation of postsynaptic G(q/11)-coupled receptors with or without Ca2+ elevation. The former pathway is independent of phospholipase C beta (PLC beta) and requires a large Ca2+ elevation to a micromolar range. The latter pathway requires PLC beta and is facilitated by a moderate Ca2+ elevation to a submicromolar range. This facilitation is caused by Ca2+ -dependency of receptor-driven PLC beta activation. The released endocannabinoids then activate presynaptic cannabinoid receptor type 1 (CB1), and suppress transmitter release from presynaptic terminals. Both CB1 receptors and G(q/11)-coupled receptors are widely distributed in the brain. Thus, the endocannabinoid-mediated retrograde modulation may be an important and widespread mechanism in the brain, by which postsynaptic events including G(q/11)-coupled receptor activation and Ca2+ elevation can retrogradely influence presynaptic function. (C) 2005 Elsevier Ltd. All rights reserved.