Society for Neuroscience Abstracts, 17, 173.9 (1991)
Abstract
To determine whether accumulation of IP is altered by manipulations that significantly alter neurotransmitter release, inositol phospholipid metabolism was examined under experimental conditions used to study acetylcholine (ACh) and dopamine (DA) release from rat neostriatal slices. Slices from Fisher 344 rats (3-mo.) were labelled with myo-2-[3H]-inositol, and IP accumulation was determined in the presence of LiCl (10 mM). Effects of nondepolarizing and depolarizing conditions, acetylcholinesterase (AChE) inhibition, and muscarinic agents were tested. Under nondepolarizing conditions, IP accumulation (% of total [3H]inositol incorporation) was 2.4 ± 0.1% (n = 3) during a 25 min incubation. If the slices were depolarized an additional 5 min following the nondepolarizing incubation, IP accumulation increased another 78% (4.28 ± 0.28%; n = 3, P < 0.05), indicating that conditions used to stimulate neurotransmitter release also increase IP accumulation. In the presence of physostigmine (PHY), an AChE inhibitor, IP accumulation following a 25 min nondepolarizing/5 min depolarizing incubation was 3.3-fold greater (P < 0.05) than in its absence. Oxotremorine-M (OXO-M), a muscarinic agonist, enhanced IP accumulation 5-fold (5 uM) and 9-fold (100 uM) during a 25 min nondepolarizing incubation, and 29% and 14% more during an additional 5 min depolarization. Pirenzepine (50 uM), a muscarinic antagonist, decreased IP accumulation in the presence of OXO-M and PHY by 74% (P < 0.01) and 68% (P < 0.01), respectively. These manipulations also significantly affected ACh and DA release, indicating that IP accumulation in neostriatal slices is significantly altered during manipulations used to study neurotransmitter release.
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