Inhibition of polyphosphoinositide turnover in rat cerebral cortex by clonidine.
In the rat brain, a number of receptors are linked to phospholipase C which catalyzes the hydrolysis of membrane inositol phospholipids; stimulation of alpha 1-adrenergic receptors, for example, increases polyphosphoinositide turnover, but stimulation of alpha 2-receptors does not. The hydrolysis of inositol phospholipids in rat cortical slices was investigated using a direct assay involving prelabeling these lipids with 3H-inositol and then measuring the formation of 3H-inositol phosphates in the presence of lithium ions. As expected, clonidine, an alpha 2-agonist, did not stimulate the formation of 3H-inositol phosphates; however, clonidine antagonized the ability of noradrenaline to stimulate 3H-inositol phosphate formation. This effect was not blocked by antagonists of alpha 2, 5HT2, H2, or muscarinic receptors. Clonidine did not affect carbachol-stimulated 3H-inositol phosphate formation.
Dyck
L E
LE
Neuropsychiatric Research Unit, University of Saskatchewan, Saskatoon, Canada.
D000818:Animals; D002217:Carbachol / Q000494:pharmacology; D002540:Cerebral Cortex / Q000187:drug effects / Q000378:metabolism*; D002852:Chromatography, Ion Exchange; D003000:Clonidine / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D006868:Hydrolysis; D007295:Inositol Phosphates / Q000037:antagonists & inhibitors / Q000378:metabolism; D008297:Male; D009638:Norepinephrine / Q000494:pharmacology; D010716:Phosphatidylinositols / Q000037:antagonists & inhibitors / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains
D007295:Inositol Phosphates; D010716:Phosphatidylinositols; D002217:Carbachol; D003000:Clonidine; D009638:Norepinephrine