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Title: Lack of inhibitory effect of aprotinin and bacitracin on the spinal release of Met-enkephalin induced by intraventricular beta-endorphin. Author: Tseng LF, King RC, Fujimoto JM. Journal: Peptides; 1986; 7(2):369-71. PubMed ID: 2426688. 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.[Abstract] [Full Text] [Related] [New Search]