Lack of inhibitory effect of aprotinin and bacitracin on the spinal release of Met-enkephalin induced by intraventricular beta-endorphin.
We have previously reported that administration of beta-endorphin intraventricularly in the rat increases the release of immunoreactive Met-enkephalin from the spinal cord. To further eliminate the possibility that the increase in Met-enkephalin might arise from the degradation of beta-endorphin injected, the effect of peptidase inhibitors, aprotinin and bacitracin, on the spinal fluid content of Met-enkephalin released by intraventricular beta-endorphin was studied using an intrathecal perfusion technique in urethane anesthetized rats. Inhibition of peptidases by intraventricular aprotinin and bacitracin did not decrease nor enhance the increased content of Met-enkephalin in the spinal perfusate produced by intraventricular beta-endorphin. The result indicates that the Met-enkephalin arises from neuronal release in the spinal cord rather than from degradation of the beta-endorphin injected intraventricularly.
D000818:Animals; D007611:Aprotinin / Q000494:pharmacology*; D001414:Bacitracin / Q000494:pharmacology*; D002552:Cerebral Ventricles / Q000187:drug effects / Q000502:physiology*; D004723:Endorphins / Q000008:administration & dosage / Q000494:pharmacology*; D004744:Enkephalin, Methionine / Q000378:metabolism*; D007276:Injections, Intraventricular; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D013116:Spinal Cord / Q000187:drug effects / Q000378:metabolism*; D001615:beta-Endorphin
D004723:Endorphins; D001414:Bacitracin; D004744:Enkephalin, Methionine; D001615:beta-Endorphin; D007611:Aprotinin