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Effects of Neuronal Activity on Inositol Phospholipid Metabolism in the Rat Autonomic Nervous System
Author(s) -
Briggs Clark A.,
Horwitz Joel,
McAfee Donald A.,
Tsymbalov Sophia,
Perlman Robert L.
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.tb12876.x
Subject(s) - inositol , sympathetic ganglion , nodose ganglion , endocrinology , superior cervical ganglion , muscarinic acetylcholine receptor , medicine , inositol phosphate , cholinergic , stimulation , chemistry , nicotinic agonist , ganglion , muscarinic antagonist , acetylcholine , biology , vagus nerve , neuroscience , receptor
The effect of nerve stimulation on inositol phospholipid hydrolysis in autonomie tissue was assessed by direct measurement of [ 3 H]inositol phosphate production in ganglia that had been preincubated with [ 3 H]inositol. Within minutes, stimulation of the preganglionic nerve increased the [ 3 H]inositol phosphate content of the superior cervical sympathetic ganglion indicating increased hydrolysis of inositol phospholipids. This effect was blocked in a low Ca 2+ , high Mg 2+ medium. It was also greatly reduced when nicotinic and muscarinic antagonists were present together in normal medium. However, neither the nicotinic antagonist nor the muscarinic antagonist alone appeared to be as effective as both in combination. In other experiments, stimulation of the vagus nerve caused dramatic increases in [ 3 H]inositol phosphate in the nodose ganglion but did not increase [ 3 H]inositol phosphate in the nerve itself. This effect was insensitive to the cholinergic antagonists. Thus, neuronal activity increased inositol phospholipid hydrolysis in a sympathetic ganglion rich in synapses, as well as in a sensory ganglion that contains few synapses. In the sympathetic ganglion, synaptic stimulation activated inositol phospholipid hydrolysis and this was primarily due to cholinergic transmission; both nicotinic and muscarinic pathways appeared to be involved.

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