β Endorphin inhibits ACh turnover in nuclei of rat brain

Abstract

NARCOTIC drugs modify cholinergic mechanisms in central and peripheral nervous systems¹, and analgesic doses of morphine, meperidine, viminol R₂ and azidomorphine decrease acetylcholine (ACh) turnover rate (TR_Ach) in selected brain nuclei^2,3. This suggests that endogenous opiate receptor agonists regulate cholinergic mechanisms in some brain nuclei². Among the endogenous opiate receptor agonists, β endorphin is particularly interesting because it is more active than morphine in causing analgesia and catalepsy⁴. This polypeptide and α endorphin share some structural similarities which correspond to fragments 61–76 and 61–91 of β lipotropin, respectively⁵. We have investigated whether α and β endorphin also mimic the action of morphine on TR_ACh of selected brain nuclei. We have found that analgesic doses of β endorphin injected intraventricularly decrease TR_ACh in cortex, hippocampus, nucleus accumbens and globus pallidus but not in nucleus caudatus. This decrease of TR_ACh was antagonised by naltrexone. In contrast, α endorphin failed to cause analgesia or to decrease TR_ACh in all brain nuclei studied.