In vivo alteration of calcium turnover induced by reserpine in rat tissues (original) (raw)

Journal of Pharmacy and Pharmacology, 1980

Abstract

when compared with rats injected acutely with saline. Since the apomorphine-induced sedation is considered to be mediated by presynaptic dopamine receptors, these data are evidence for the development of presynaptic supersensitivity following chronic haloperidol. Higher doses of apomorphine elevated locomotor activity to presedative levels indicating an activation of supersensitive postsynaptic dopamine receptors. In addition 2 out of 5 rats displayed obvious stereotypic behaviour. Combined injection of haloperidol and lithium daily for 34 days reversed the preand postsynaptic supersensitive responses to apomorphine. Apomorphine at 0.004 and 0.008 mg kg-' did not induce significant inhibition of locomotor activity as was seen in rats treated chronically with only haloperidol (Fig. 1). This supports previous electrophysiological data suggesting that lithium blocks the development of presynaptic dopamine receptor supersensitivity. The higher doses of apomorphine did not produce increases in locomotor activity in chronic haloperidol plus lithium treated rats (Fig. 1). On the contrary apomorphine (0.01 6 mg kg-l) induced sedation that was analogous to the responses seen in the control groups. In conclusion lithium appears to block the develop. ment of supersensitivity in both preand postsynaptic dopamine receptors. The chronic lithium regimen has been demonstrated to result in plasma lithium concen. trations in the therapeutic range of lithium in man (Allikments et al 1979). Therefore the stabilization of preand postsynaptic receptors by lithium may repre. sent an important mechanism in the clinical pharmacotherapy of manic-depressive disorders and tardive dyskinesia. February 1 , 1980

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