Abstract
We investigated whether GABA activates phospholipase A 2 (PLA 2) during acrosomal exocytosis, and if the MEK-ERK1/2 pathway modulates PLA 2 activation initiated by GABA, progesterone or zona pellucida (ZP). In guinea pig spermatozoa prelabelled with [ 14C]arachidonic acid or [ 14C]choline chloride, GABA stimulated a decrease in phosphatidylcholine (PC), and release of arachidonic acid and lysoPC, during exocytosis. These lipid changes are indicative of PLA 2 activation and appear essential for exocytosis since inclusion of aristolochic acid (a PLA 2 inhibitor) abrogated them, along with exocytosis. GABA activation of PLA 2 seems to be mediated, at least in part, by diacylglycerol (DAG) and protein kinase C since inclusion of the DAG kinase inhibitor R59022 enhanced PLA 2 activity and exocytosis stimulated by GABA, whereas exposure to staurosporine decreased both. GABA-, progesterone- and ZP-induced release of arachidonic acid and exocytosis were prevented by U0126 and PD98059 (MEK inhibitors). Taken together, our results suggest that PLA 2 plays a fundamental role in agonist-stimulated exocytosis and that MEK-ERK1/2 are involved in PLA 2 regulation during this process.
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call