Regulation of somatodendritic dopamine release by corticotropin-releasing factor via the inhibition of voltage-operated Ca2+ channels
Regulation of somatodendritic dopamine release by corticotropin-releasing factor via the inhibition of voltage-operated Ca2+ channels
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DOI：
10.1016/j.neulet.2009.08.066
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发表时间：
2009-11-06
影响因子：
2.5
通讯作者：
Chung, Sungkwon
中科院分区：
文献类型：
--
作者：
Kim, Yonjung;Park, Myoung Kyu;Chung, Sungkwon
黑质致密部的多巴胺（DA）神经元从它们的躯体和树突释放DA，从而调节运动活动和肌肉张力。之前，我们报道了Ca2+通过电压操作的Ca2+通道（vocc）内流有助于自发的体树突DA释放。由于促肾上腺皮质激素释放因子（CRF）调节VOCC，我们试图用电流法确定尿皮质素是否影响离体DA神经元的体树突DA释放。尿皮质素的应用通过激活1型CRF受体可逆地抑制了VOCC和DA释放事件的频率。L型和t型Ca2+通道的阻滞剂有效地消除了尿皮质素对DA释放事件频率和Ca2+电流的影响。这些结果表明，CRF通过抑制L-和t型Ca2+通道抑制体树突DA释放。因此，应激激素抑制体树突DA的释放可能是应激对运动功能影响的分子机制之一。2009爱思唯尔爱尔兰有限公司版权所有。
Dopamine (DA) neurons in the substantia nigra pars compacta release DA from their somata and dendrites, which regulate motor activity and muscle tone. Previously, we reported that Ca2+ influx through voltage-operated Ca2+ channels (VOCCs) contributes to spontaneous somatodendritic DA release. Since corticotropin-releasing factor (CRF) regulates VOCC, we sought to determine whether urocortin affects somatodendritic DA release in the isolated DA neurons using amperometry method. The application of urocortin reversibly inhibited both VOCC and the frequency of DA release events via the activation of type-1 CRF receptor. The blockers for L- and T-type Ca2+ channels effectively abolished the effects of urocortin both on the frequency of DA release events and on Ca2+ current. These results indicate that CRF inhibits somatodendritic DA release by inhibiting L- and T-type Ca2+ channels. Thus, the inhibition of somatodendritic DA release by stress hormone may be one of the molecular mechanisms underlying the effect of stress on motor function. (C) 2009 Elsevier Ireland Ltd. All rights reserved.