Role of putative neurotransmitters in bradykinin-induced catalepsy in the rat.

Abstract

Intracerebroventricular administration of bradykinin produced a dose-related cataleptic response in rats. Bradykinin-induced catalepsy was significantly attenuated following pretreatment with pharmacologic agents that decrease central prostaglandin, serotonin, and acetylcholine activity, as well as by the opioid receptor antagonist naloxone. Conversely, pharmacologic treatments that enhance central catecholamine levels and, specifically, central dopaminergic activity also inhibited bradykinin-induced catalepsy. The prostaglandin precursor, arachidonic acid, and prostaglandin E2, as well as met- and leu-enkephalin showed a synergistic effect with bradykinin catalepsy. Much evidence indicates that several actions of bradykinin, in the central nervous system and the periphery, are likely to be prostaglandin mediated. Further, the recent report from this laboratory that centrally administered bradykinin specifically augments rat brain prostaglandin E2 levels, together with the proposed role of central prostaglandins as modulators of central synaptic transmission, suggests that bradykinin-induced catalepsy is mediated and modulated through PGE effects on serotonergic, cholinergic, and dopaminergic neurotransmitter systems. The study also indicates that endogenous opioid peptides may be involved in braydkinin catalepsy.