Effects of Neuronal Activity on Inositol Phospholipid Metabolism in the Rat Autonomic Nervous System |
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Authors: | Clark A Briggs Joel Horwitz† Donald A McAfee Sophia Tsymbalov† Robert L Perlman† |
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Institution: | Division of Neurosciences, Beckman Research Institute of the City of Hope, Duarte, California, U.S.A.;Department of Physiology and Biophysics, College of Medicine, University of Illinois, Chicago, Illinois, U.S.A. |
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Abstract: | The effect of nerve stimulation on inositol phospholipid hydrolysis in autonomic tissue was assessed by direct measurement of 3H]inositol phosphate production in ganglia that had been preincubated with 3H]inositol. Within minutes, stimulation of the preganglionic nerve increased the 3H]inositol phosphate content of the superior cervical sympathetic ganglion indicating increased hydrolysis of inositol phospholipids. This effect was blocked in a low Ca2+, high Mg2+ 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 3H]inositol phosphate in the nodose ganglion but did not increase 3H]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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Keywords: | Phosphatidylinositol Neuronal activity Superior cervical ganglion Nodose ganglion Nicotinic transmission Muscarinic transmission |
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