Carbachol-stimulated release of arachidonic acid and eicosanoids from brain cortex synaptoneurosome lipids of adult and aged rats.

摘要: Synaptoneurosomes from the brain cortex of adult rats (4 months old) and aged (27 old), prelabeled with [14C]arachidonic acid (AA), were used as source enzyme(s) substrates to study effect a cholinergic agonist on release AA eicosanoids. In synaptoneurosomes brains, carbachol, nonhydrolyzable analog acetylcholine, increased by 16% in presence 2 mM calcium. This agonist-mediated occurred specifically phosphatidylinositol (PI). Concomitantly, carbachol Ca2+significantly activated formation 15-HETE PGF2 α. level eicosanoids was also observed endogenous had no The results studies involving inhibitors phospholipase A2 (PLA2) C (PLC) suggested that PLA2 is almost completely responsible for Ca2+-dependent, carbachol-mediated liberation. distribution labeled lipids after incubation Mm Ca2+ indicated synaptoneurosomes, muscarinic receptor-mediated degradation phosphoinositides through preserved, but turnover phosphoinositide cycle probably suppressed. These indicate aging significantly affects population cholinergic-muscarinic receptors coupled PLA2.