Electrophysiological evidence for involvement of cyclic adenosine monophosphate in dopamine responses of caudate neurons

Abstract

Microiontophoresis of dopamine, apomorphine, cyclic adenosine monophosphate (cyclic AMP) and monobutyryl cyclic AMP depresses tile spontaneous or drug-evoked discharge of the majority of neurons in the rat caudate nucleus. Responses to dopamine are enhanced only slightly by the phosphodiesterase (PDE) inhibitors aminophylline or papaverine, both of which also directly slow caudate neurons. However, iontophoresis of the PDE inhibitor methyl isobutyl xanthine (IBMX), or combination of IBMX and papaverine produced marked potentiations of dopamine-induced inhibitions. IBMX alone has little or no direct actions. Chlorpromazine, but not tile beta adrenergic biocker MJ-1999, antagonized dopamine, but not cyclic AMP responses. After destruction of tile nigral striatal dopamine bundle by focal injection of 6-hydroxydopamine, caudate neurons show supersensitivity to dopamine and apomorphine. These results provide electrophysiological support for the hypothesis that the dopamine receptor in caudate may be functionally related to tile adenyl cyclase system, as suggested by recent biochemical findings.