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Neurotransmitter‐Induced Inositol Phosphate Formation in Neurons in Primary Culture
Author(s) -
Weiss Samuel,
Schmidt Bernard H.,
Sebben Michèle,
Kemp Dorothy E.,
Bockaert Joël,
Sladeczek Fritz
Publication year - 1988
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.1471-4159.1988.tb03026.x
Subject(s) - carbachol , inositol phosphate , glutamate receptor , inositol , neurotransmitter , neurotensin , biology , medicine , endocrinology , norepinephrine , microbiology and biotechnology , chemistry , receptor , stimulation , biochemistry , neuropeptide , dopamine
Inositol‐1,4,5‐trisphosphate, produced in cells as a breakdown product of phosphatidylinositol‐4,5‐bisphosphate, induces, in many cell types, release of calcium from intracellular stores. In murine striatal neurons, differentiated in primary culture, carbachol, norepinephrine, glutamate, and neurotensin stimulate 3 H‐labeled inositol phosphate ( 3 H‐IP) production. The glutamate response was recently characterized as being mediated primarily by receptors of the quisqualate subtype. In the present study, we found that major differences exist between glutamate‐stimulated 3 H‐IP formation and those stimulated by the other neuromediators. The maximal response to glutamate occurred before and during synaptogenesis and declined thereafter, whereas the maximal response to either carbachol or norepinephrine required complete neuronal differentiation. Although the glutamate response appears to be mediated exclusively by direct interaction with the neuro‐transmitter receptors, responses to carbachol, norepinephrine, and neurotensin were partially or completely blocked by tetrodotoxin.