Aghajanian G K, Wang Y Y
Brain Res. 1986 Apr 23;371(2):390-4. doi: 10.1016/0006-8993(86)90382-3.
Pertussis toxin, a substance known to inactivate the inhibitory guanine nucleotide regulatory unit of adenylate cyclase, was injected into the lateral cerebral ventricle of rats; intracellular recordings were made from locus coeruleus neurons in brain slices 1-3 days later. Morphine (an opiate agonist) and clonidine (an alpha 2-agonist) produced the expected outward currents (and associated hyperpolarization and inhibition of firing) in controls whereas the effects of both agonists were blocked in animals pretreated with pertussis toxin. These results are consistent with the hypothesis that opiate and alpha 2-agonists may depress the firing of locus coeruleus neurons by inhibiting adenylate cyclase via a guanine nucleotide regulatory protein.
百日咳毒素是一种已知能使腺苷酸环化酶的抑制性鸟嘌呤核苷酸调节单位失活的物质，将其注入大鼠侧脑室；1至3天后在脑片中对蓝斑神经元进行细胞内记录。在对照组中，吗啡（一种阿片类激动剂）和可乐定（一种α2激动剂）产生了预期的外向电流（以及相关的超极化和放电抑制），而在预先用百日咳毒素处理的动物中，两种激动剂的作用均被阻断。这些结果与以下假设一致，即阿片类药物和α2激动剂可能通过鸟嘌呤核苷酸调节蛋白抑制腺苷酸环化酶，从而抑制蓝斑神经元的放电。
