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Activation of phosphoinositide turnover and protein kinase C by neurotransmitters that modulate calcium channels in embryonic chick sensory neurons
Author(s) -
Harish O.E.,
Role L.W.
Publication year - 1992
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/0736-5748(92)90032-u
Subject(s) - neurotransmitter , biology , pertussis toxin , neurotransmitter receptor , protein kinase c , microbiology and biotechnology , voltage dependent calcium channel , gabab receptor , sensory neuron , calcium , protein kinase a , medicine , endocrinology , neuroscience , receptor , g protein , signal transduction , kinase , biochemistry , gabaa receptor
Gamma aminobutyric acid (GABA) and norepinephrine modulate the excitability of primary chick sensory neurons by decreasing the voltage dependent Ca current. Although previous electro‐physiological studies indicate that neurotransmitter modulation of the Ca current in these neurons involves protein kinase C, the biochemical aspects of this mechanism have not been examined directly. We find that both norepinephrine (via a unique a receptor subtype) and GABA (via GABA b receptors) linked to pertussis toxin sensitive pathways, stimulate the metabolism of membrane phosphatidylinositol phospholipids in primary chick sensory neurons. In addition, norepinephrine causes the rapid translocation of C kinase activity from cytosolic to membrane associated distribution, consistent with its rapid activation in response to applied neurotransmitter. The pharmacology, pertussis toxin sensitivity and time course of the biochemical changes due to neurotransmitter treatment parallel the effects of these transmitters on calcium current modulation. These biochemical studies confirm the hypothesis that activation of protein kinase C is critically involved in calcium channel modulation in embryonic chick sensory neurons.