Ambrósio A F, Malva J O, Carvalho A P, Carvalho C M
Department of Zoology and Faculty of Medicine, University of Coimbra, Portugal.
Neurosci Lett. 1996 Dec 20;220(3):163-6. doi: 10.1016/s0304-3940(96)13252-3.
We determined that activation of adenosine A1 receptors in striatal synaptosomes with 100 nM N6-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 A1 receptors.
我们确定，用100 nM N6-环戊基腺苷（CPA）激活纹状体突触体中的腺苷A1受体，可分别抑制内源性谷氨酸的释放以及因4-氨基吡啶（4-AP）刺激而导致的细胞内游离Ca2+浓度（[Ca2+]i）升高，抑制率分别为28%和19%。此外，CPA增强了ω-芋螺毒素GVIA（ω-Cgtx GVIA）、ω-芋螺毒素MVIIC或ω-芋螺毒素GVIA加ω-芋螺毒素MVIIC对内源性谷氨酸释放的抑制作用。在[Ca2+]i信号中也观察到了类似的效应。CPA和ω-芋螺毒素GVIA的抑制作用是相加的，但CPA和ω-芋螺毒素MVIIC的作用只是部分相加。这些结果表明，与谷氨酸释放相关的P/Q型Ca2+通道和其他类型的Ca2+通道在腺苷A1受体激活后受到抑制。
