Phosphatidylinositol degradation in ischemic brain specifically activated by synaptosomal enzymes.
The effect of ischemia on phosphatidylinositol (PI) degrading enzymes in brain homogenate, cytosol and synaptosomes was investigated to evaluate the involvement of cholinergic receptor in PI hydrolysis during ischemia. The activity of phospholipase C in cytosol was not changed by ischemic insult. PI degradation in synaptosomes was significantly (60%) enhanced by ischemia. Atropine and gamma-butyrolactone abolished the ischemic effect on PI degradation, suggesting that the cholinergic receptor system mediates breakdown of PI during ischemia.
D015107:4-Butyrolactone / Q000494:pharmacology; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D002545:Brain Ischemia / Q000378:metabolism*; D003600:Cytosol / Q000201:enzymology; D005849:Gerbillinae; D010716:Phosphatidylinositols / Q000378:metabolism*; D011950:Receptors, Cholinergic / Q000187:drug effects / Q000378:metabolism; D013574:Synaptosomes / Q000201:enzymology*; D010738:Type C Phospholipases / Q000378:metabolism
D010716:Phosphatidylinositols; D011950:Receptors, Cholinergic; D001285:Atropine; D010738:Type C Phospholipases; D015107:4-Butyrolactone