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Tryptamine Induces Phosphoinositide Turnover and Modulates Adrenergic and Muscarinic Cholinergic Receptor Function in Cultured Cerebellar Granule Cells
Author(s) -
Ishitani Ryoichi,
Kimura Mitsutoshi,
Takeichi Masami,
Chuang DeMaw
Publication year - 1994
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 - 10.1046/j.1471-4159.1994.63062080.x
Subject(s) - tryptamine , carbachol , endocrinology , prazosin , medicine , chemistry , muscarinic acetylcholine receptor , oxotremorine , cholinergic , biology , biochemistry , receptor , antagonist
Tryptamine dose‐dependently increased phosphoinositide (PI) hydrolysis by approximately fourfold in primary cultures of rat cerebellar granule cells (EC 50 = 56 µ M ). The PI response stimulated by tryptamine was dependent on the presence of extracellular Ca 2+ and Na + . Tryptamine‐induced PI breakdown could be partially inhibited by pretreatment with 4β‐phorbol 12‐myristate 13‐acetate but not pertussis toxin. The presence of tryptamine markedly attenuated PI responses induced by norepinephrine (NE) and carbachol, with no apparent effect on the responses to 5‐hydroxytryptamine and glutamate. The inhibition of NE‐ and carbachol‐induced PI turnover by tryptamine was dose dependent with IC 50 values of ∼0.4 and ∼2.5 m M , respectively. Pretreatment of cells with tryptamine (0.5 m M ) also attenuated NE‐ and carbachol‐induced PI turnover, but failed to affect 5‐hydroxytryptamine‐ and glutamate‐induced responses. Furthermore, ketanserin, atropine, and prazosin did not have any effect on inositol phosphate formation induced by tryptamine. These observations indicate that tryptamine markedly increased Ca 2+ ‐ and Na + ‐dependent PI turnover in cerebellar neurons and selectively inhibited NE‐ and carbachol‐induced PI hydrolysis.