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Phospholipase C activation induced by noradrenaline in rat hippocampal slices is potentiated by GABA‐receptor stimulation.
Author(s) -
Ruggiero M.,
Corradetti R.,
Chiarugi V.,
Pepeu G.
Publication year - 1987
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1002/j.1460-2075.1987.tb02405.x
Subject(s) - biology , stimulation , hippocampal formation , phospholipase , receptor , gabaa receptor , phospholipase c , phospholipase a , phospholipase d , neuroscience , pharmacology , endocrinology , microbiology and biotechnology , medicine , phospholipase a2 , biochemistry , signal transduction , enzyme
We have studied the effect of gamma‐aminobutyric acid (GABA) and other GABA‐receptor agonists (3‐aminopropanesulphonic acid and muscimol) on the noradrenaline‐induced stimulation of polyphosphoinositide metabolism in rat hippocampal slices. Formation of water‐soluble inositol phosphates, and polyphosphoinositide metabolism were studied in hippocampal slices prelabelled with [3H]myoinositol. Noradrenaline induced formation of inositol mono‐, bis‐ and trisphosphate during 10 min incubation in the presence of lithium; activation of phospholipase C by noradrenaline was also reflected by the hydrolysis of polyphosphoinositides and by the increased metabolism of phosphatidylinositol. GABA‐receptor agonists were unable to activate per se phospholipase C; however, when added together with a low concentration of noradrenaline, they greatly potentiated the noradrenaline‐stimulated polyphosphoinositide metabolism. We conclude that GABA‐receptor agonists potentiate the effect of noradrenaline on polyphosphoinositide turnover and we discuss the role of this neurotransmitter interaction in the physiology of the hippocampus.