Modulation of Ca2+ channels by activation of adenosine A(1) receptors in rat striatal glutamatergic nerve terminals
Modulation of Ca2+ channels by activation of adenosine A(1) receptors in rat striatal glutamatergic nerve terminals
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DOI：
10.1016/s0304-3940(96)13252-3
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发表时间：
1996-12-20
影响因子：
2.5
通讯作者：
Carvalho, CM
中科院分区：
文献类型：
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作者：
Ambrosio, AF;Malva, JO;Carvalho, CM
用100 nM N-6-环戊基腺苷(CPA)激活纹状体突触体内的腺苷A(1)受体，可抑制由4-氨基吡啶(4-AP)刺激引起的内源性谷氨酸的释放和细胞内游离钙浓度([Ca~(2+)](I)的升高，分别为28%和19%)。此外，CPA还增强了omega-Cgtx GVIA(omega-Cgtx GVIA)、omega-Cgtx MVIIC或omega-Cgtx GVIA+omega-Cgtx MVIIC对内源谷氨酸释放的抑制作用。在[Ca~(2+)](I)信号中也观察到类似的效应。CPA和omega-Cgtx GVIA的抑制作用是相加的，而CPA和omega-Cgtx MVIIC的抑制作用是部分相加的。这些结果表明，激活腺苷A(1)受体后，与谷氨酸释放有关的P/Q型钙通道和其他类型的钙通道(S)(S)被抑制。(C)1996年爱思唯尔爱尔兰科学有限公司。
We determined that activation of adenosine A(1) receptors in striatal synaptosomes with 100 nM N-6-cyclopentyladenosine (CPA) inhibited both the release of endogenous glutamate and the increase of intracellular free Ca2+ concentration ([Ca2+](i)), due to 4-aminopyridine (4-AP) stimulation, by 28 and 19%, respectively. Furthermore, CPA enhanced the inhibition of endogenous glutamate release due to omega-conotoxin GVIA (omega-Cgtx GVIA), omega-Cgtx MVIIC or omega-Cgtx GVIA plus omega-Cgtx MVIIC. Similar effects were observed in the [Ca2+](i) signal. The inhibitory effects of CPA and omega-Cgtx GVIA were additive, but the effects of CPA and omega-Cgtx MVIIC were only partially additive. These results suggest that P/Q-type Ca2+ channels and other type(s) of Ca2+ channel(s), coupled to glutamate release, are inhibited subsequently to activation of adenosine A(1) receptors. (C) 1996 Elsevier Science Ireland Ltd.