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Manganese Stimulates the Incorporation of [ 3 H]Inositol into a Pool of Phosphatidylinositol in Brain That Is Not Coupled to Agonist‐Induced Hydrolysis
Author(s) -
Schoepp Darryle D.
Publication year - 1985
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1985.tb07216.x
Subject(s) - inositol , carbachol , phosphatidylinositol , chemistry , phospholipase c , agonist , inositol phosphate , hydrolysis , stimulation , pi , endocrinology , biochemistry , receptor , medicine , biology , signal transduction
Mn 2+ greatly increases the incorporation of myo ‐[ 3 H]inositol into phosphatidylinositol (PI) of brain and other tissues by stimulating the activity of a PI‐ myo inositol exchange enzyme. This study examined the ability of norepinephrine (NE) and carbachol to stimulate the hydrolysis of [ 3 H]PI formed in the absence and presence of Mn 2+ ‐stimulated [ 3 H]inositol exchange. Rat cerebral cortical slices were incubated with myo ‐[ 3 H]inositol for 60 min in an N ‐2‐hydroxyethyl piperazine‐ N′ ‐2‐ethanesulfonic acid (HEPES) buffer without or with MnCl 2 (1 m M ). The tissue was washed and further incubated with unlabeled myo ‐inositol and LiCl (10 m M ). Prelabeled slices were then incubated with NE (0.1 m M ) or carbachol (1 m M ) to induce agonist‐stimulated [ 3 H]PI hydrolysis. Mn 2+ treatment resulted in eight‐ and sixfold increases in control levels of [ 3 H]PI and [ 3 H]inositol monophosphate ([ 3 H]IP), respectively. Both NE and carbachol stimulated [ 3 H]IP formation in tissue prelabeled without or with manganese. However, the degree of stimulation (percentage of control values) was greatly attenuated in the presence of Mn 2+ . In the absence of Mn 2+ treatment, NE decreased [ 3 H]PI radioactivity in the tissue to 80% of control values. However, NE did not decrease [ 3 H]PI radioactivity in the Mn 2+ ‐treated tissue. These data demonstrate that Mn 2+ stimulates incorporation of myo ‐[ 3 H]inositol into a pool of PI in brain that has a rapid turnover but is not coupled to agonist‐induced hydrolysis.