Sumners C, Woodruff G N, Poat J A
Psychopharmacology (Berl). 1981;73(2):180-3. doi: 10.1007/BF00429214.
A study was made of the effects of manipulating brain dopaminergic activity upon drinking induced by intracerebroventricular administration of angiotensin II or carbachol. Non-specific lesions induced by injecting 6-hydroxydopamine (6-OHDA) into the cerebroventricles caused a significant reduction in angiotensin-induced thirst without affecting carbachol drinking. specific 6-OHDA-induced lesions of the dopaminergic nigro-striatal pathway also attenuated the angiotensin-induced response, while unilateral lesions reduced and bilateral lesions almost completely abolished the effect. Again, the response to carbachol was unaffected. Chronic haloperidol treatment increased behavioural responses to the dopamine agonist apomorphine and significantly stimulated angiotensin-induced drinking without affecting response to carbachol. These studies provide support for the hypothesis that a dopaminergic event is involved in the angiotensin-induced thirst response and point to the need for a functioning dopaminergic nigro-striatal pathway for the full expression of this response.
研究了操纵脑多巴胺能活性对脑室内注射血管紧张素 II 或卡巴胆碱诱导的饮水的影响。向脑室注射 6-羟基多巴胺(6-OHDA)诱导的非特异性损伤导致血管紧张素诱导的口渴显著减少,而不影响卡巴胆碱诱导的饮水。多巴胺能黑质-纹状体通路的特异性 6-OHDA 诱导损伤也减弱了血管紧张素诱导的反应,而单侧损伤降低了该效应,双侧损伤几乎完全消除了该效应。同样,对卡巴胆碱的反应未受影响。慢性氟哌啶醇治疗增加了对多巴胺激动剂阿扑吗啡的行为反应,并显著刺激了血管紧张素诱导的饮水,而不影响对卡巴胆碱的反应。这些研究为多巴胺能事件参与血管紧张素诱导的口渴反应这一假说提供了支持,并指出需要一个功能正常的多巴胺能黑质-纹状体通路来充分表达这种反应。