Adenosine A3 receptors potentiate hippocampal calcium current by a PKA-dependent/PKC-independent pathway.
Adenosine A3 receptors potentiate hippocampal calcium current by a PKA-dependent/PKC-independent pathway.
复制标题
腺苷 A3 受体通过 PKA 依赖性/PKC 独立途径增强海马钙电流。
DOI：
10.1016/s0028-3908(97)83762-8
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发表时间：
1997
影响因子：
4.7
通讯作者：
Mogul,DJ
中科院分区：
文献类型：
--
作者：
Fleming,KM;Mogul,DJ
在急性分离的豚鼠海马CA 3区锥体神经元上，用电压钳方法研究腺苷受体对高阈值钙电流（伊卡）的调制。当这些神经元在A1、A2 a和A2 b受体拮抗剂存在的情况下暴露于腺苷时，在测试电位为-10 mV时发生ICa增强，但在-40 mV时不发生。A3激动剂N6-2-（4-aminophenyl）ethyl-adenosine（APNEA）单独或与A1和A2拮抗剂联合使用时也有类似的增强作用。推定的A4激动剂2-苯基氨基腺苷（CV-1808; Cornfield等人，1992）在25 nM和2500 nM之间的四种测试浓度下不增强ICa。对于呼吸暂停诱导的K0.5 Zhou等人，1992年）。细胞内应用WIPTIDE（一种PKA抑制剂）可阻断APNEA的ICA增强作用（p < 0.001），但不受蛋白激酶C（PKC）抑制肽的影响（19-36）。这些结果表明：（1）A3受体活化可显著增强伊卡，和（2）因为A3受体与腺苷酸环化酶的下调有关（Zhou等人，1992），PKA似乎与伊卡负偶联。© 1997 Elsevier Science Ltd.保留所有权利。
The modulation of high-threshold Ca current (ICa) by adenosine receptors was studied using the voltage clamp method on acutely dissociated guinea pig hippocampal CA3 pyramidal neurons. When these neurons were exposed to adenosine in the presence of A1, A2aand A2breceptor antagonists, ICapotentiation occurred at test potentials of −10 mV, but not at −40 mV. Similar potentiation also occurred using the A3agonist N6-2-(4-aminophenyl)ethyl-adenosine (APNEA), either alone or in the presence of A1and A2antagonists. The putative A4agonist 2-phenylaminoadenosine (CV-1808; Cornfield et al., 1992) did not potentiate ICaat four concentrations tested between 25 nM and 2500 nM. K0.5for the APNEA-induced Zhou et al., 1992). ICapotentiation by APNEA was blocked by intracellular application of WIPTIDE, a PKA inhibitor (p < 0.001), but was not affected by protein kinase C (PKC) inhibitor peptide (19–36). These results indicate that: (1) A3receptor activation can significantly potentiate ICa, and (2) because the A3receptor has been linked to down-regulation of adenylyl cyclase (Zhou et al., 1992), PKA appears to be negatively coupled to ICa. © 1997 Elsevier Science Ltd. All rights reserved.