Beta-endorphin C-terminal peptide evokes arachidonic acid release from cortical neurones.
The release of free [3H]arachidonic acid and its metabolites (AAM) from mouse embryo cortical neurones cultured in serum-free medium stimulated by beta-endorphin C-terminal dipeptide (glycl-L-glutamine, Gly-Gln) was investigated. Gly-Gln but not the related dipeptide, glycyl-glutamic acid, caused a 2-fold elevation of AAM release which was blocked in the absence of extracellular calcium, in the presence of 5 mM magnesium and by the phospholipase A2 (PLA2) inhibitor, mepacrine. Other proopiomelanocortin (POMC) peptides did not elicit AAM release. The response to Gly-Gln was unaffected by D-amino-2-phospho-5-valeric acid (AP5) and 7-chlorokynurenic acid (7-ClKY), antagonists respectively at the ligand and allosteric glycine binding sites of the NMDA glutamate receptor subtype. However, it was inhibited in a dose-dependent manner by antagonists at the phencyclidine (PCP) and sigma sites. The results suggest that Gly-Gln causes AAM release by activating PLA2 through the mediation of a PCP/sigma-like receptor.
Haynes
L
L
Department of Zoology, University of Bristol, U.K.
D000818:Animals; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000378:metabolism*; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000187:drug effects* / Q000196:embryology / Q000378:metabolism; D004151:Dipeptides / Q000494:pharmacology*; D051379:Mice; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*
D001095:Arachidonic Acids; D004151:Dipeptides; C039788:glycylglutamine; D016718:Arachidonic Acid