| Abstract: | 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. |
