Mogul D J, Adams M E, Fox A P
Department of Pharmacological and Physiological Sciences, University of Chicago, Illinois 60637.
Neuron. 1993 Feb;10(2):327-34. doi: 10.1016/0896-6273(93)90322-i.
Adenosine is released in the brain in significant quantities in response to increased cellular activity. Adenosine has been shown either to decrease synaptic transmission or to produce an excitatory response in hippocampal synapses, resulting in increased glutamate release. Previous reports have shown that adenosine or its analogs reduced Ca2+ current in dorsal root ganglion and hippocampal neurons. Here we show that the selective activation of adenosine receptor subtypes has different effects on Ca2+ channels from acutely isolated pyramidal neurons from the CA3 region of guinea pig hippocampus. Activation of A1 receptors inhibited primarily N-type Ca2+ current. In contrast, activation of A2b receptors resulted in significant potentiation of P-type but not N-type Ca2+ current. This potentiation could be inhibited by blocking the cAMP-dependent protein kinase. Because of the ubiquity of adenosine, the differential effects on Ca2+ channels of adenosine receptor subtype activation may have significant implications for neuronal excitability.
腺苷在大脑中会因细胞活动增加而大量释放。研究表明，腺苷既能减少突触传递，也能在海马突触中产生兴奋性反应，导致谷氨酸释放增加。此前的报道显示，腺苷或其类似物可降低背根神经节和海马神经元中的Ca2+电流。在此我们表明，腺苷受体亚型的选择性激活对豚鼠海马CA3区急性分离的锥体神经元的Ca2+通道有不同影响。A1受体的激活主要抑制N型Ca2+电流。相反，A2b受体的激活导致P型而非N型Ca2+电流显著增强。这种增强可通过阻断cAMP依赖性蛋白激酶来抑制。由于腺苷无处不在，腺苷受体亚型激活对Ca2+通道的不同影响可能对神经元兴奋性有重要意义。
