Effects of specific dopamine lesions and dopamine receptor sensitivity on angiotensin II- and carbachol-induced thirst in rats

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.     

Behavioural and neurochemical studies on apomorphine-induced hypomotility in mice

Small doses of apomorphine (0.075–0.60 μmol/kg), injected subcutaneously into mice, elicited a strong hypomotive response of 20 to 30 min duration. This effect could be inhibited not only by neuroleptics, such as pimozide or sulpiride, but was also partly antagonized by the α-adrenergic antagonists, yohimbine and piperoxane. Other drugs, such as prazosin, methysergide and bicuculline were completely inactive in antagonizing apomorphine hypomotility. Yohimbine (0.25 μmol/kg) did not affect striatal dihydroxyphenylacetic acid (DOPAC) levels nor did it antagonize the apomorphine-induced fall in DOPAC concentrations. In addition, yohimbine did not antagonize the inhibitory effect of apomorphine on the γ-butyrolactone-induced rise in dopamine (DA) levels. These results show that at this dose yohimbine was not having a significant effect on pre- or postsynaptic DA receptors. Apomorphine was, however, shown to alter noradrenaline turnover. It appears, therefore, that yohimbine may inhibit apomorphine-induced hypomotility by acting at α₂-adrenergic receptors and that, in addition to dopaminergic receptors, noradrenergic systems may be involved in apomorphine-induced hypomotility.