Handley S L, Singh L
Neuropharmacology. 1986 Dec;25(12):1315-21. doi: 10.1016/0028-3908(86)90102-4.
Head-twitching in rats induced by quipazine was reduced by bilateral lesions of the locus coeruleus (LC) produced by 6-hydroxydopamine. Both beta 1-and beta 2-adrenoceptor agonists potentiated the head-twitch induced by quipazine in sham-operated controls. Lesions of the locus coeruleus increased the responses to the beta 1-adrenoceptor agonists, prenalterol and dobutamine, but reduced the response to the beta 2-adrenoceptor agonists, salbutamol and procaterol. Diazepam (0.25 mg/kg) also potentiated the response to quipazine and this was reversed to inhibition by lesions of the locus coeruleus. These results suggest that the beta 1-adrenoceptors involved are postsynaptic and the beta 2-adrenoceptors are presynaptic to neurones of the locus coeruleus and indicate a dual action of diazepam on the head-twitch induced by quipazine. Possible mechanisms for these effects are discussed.
6-羟基多巴胺造成的蓝斑(LC)双侧损伤可减轻喹哌嗪诱导的大鼠头部抽搐。在假手术对照组中,β1和β2肾上腺素能受体激动剂均可增强喹哌嗪诱导的头部抽搐。蓝斑损伤增强了对β1肾上腺素能受体激动剂普瑞特罗和多巴酚丁胺的反应,但减弱了对β2肾上腺素能受体激动剂沙丁胺醇和丙卡特罗的反应。地西泮(0.25毫克/千克)也增强了对喹哌嗪的反应,而蓝斑损伤可将这种增强作用逆转至抑制作用。这些结果表明,所涉及的β1肾上腺素能受体位于突触后,β2肾上腺素能受体位于蓝斑神经元的突触前,并表明地西泮对喹哌嗪诱导的头部抽搐具有双重作用。文中讨论了这些效应的可能机制。