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A S Bhave

Publications and source records attributed to A S Bhave.

5 recordsLinked to original sources
PubMed1991

Depolarizing stimuli and neurotransmitters utilize separate pathways to activate protein kinase C in sympathetic neurons.

Several types of extracellular signals affect the function of peripheral neurons. Depolarizing stimuli cause sudden increases in permeability to various ions leading to propagation of nerve impulses and release of transmitter substances. Neurons also receive external signals via neurotransmitter receptors located on the membrane. Different types of receptors present on sympathetic neurons are believed to modulate stimulation-evoked release of norepinephrine. We have investigated the effects of depolarizing stimuli and neurotransmitters on different signaling pathways in homogeneous cultures of chick sympathetic neurons. Depolarizing stimuli (35 mM KCl; electrical stimulation, 1 Hz for 5 min) and neurotransmitters (acetylcholine and 5-hydroxytrypatmine) enhanced membrane binding of protein kinase C by 2-5-fold. 35 mM KCl increased formation of 1,2-diacylglycerol and hydrolysis of [3H]phosphatidycholine without affecting [3H] phosphoinositide hydrolysis. Neurotransmitters increased [3H]inositol phosphates and 1,2-diacylglycerol without affecting the hydrolysis of [3H]phosphatidylcholine. 5-Hydroxytryptamine and acetylcholine (muscarinic component) did not increase Ca2+ concentration in the Indo-1-loaded neuronal cell body or the growth cone, but 35 mM KCl and electrical stimulation caused a marked increase in Ca2+ concentration in both regions of sympathetic neurons. We believe this to be the first demonstration of these two types of signalling mechanisms co-existing in sympathetic neurons; depolarization activate the phosphatidylcholine pathway and neurotransmitters activate the phosphatidylinositol pathway. The importance of two pathways in controlling neuronal Ca2+ concentration and the release of transmitter is discussed.

Animals↗
PubMed1991

Activation of muscarinic and serotonergic receptors results in phosphoinositide hydrolysis but not in mobilization of calcium in sympathetic neurons.

The effects of various neurotransmitters on phosphoinositide hydrolysis, mobilization of Ca2+ and release of [3H]-norepinephrine ([3H]-NE) were studied in cultures of sympathetic neurons of chick embryos. [3H]-inositol-1,4,5-triphosphate ([3H]-IP3) was increased in sympathetic neurons by acetylcholine (ACh), muscarine and serotonin (5-HT). Dopamine and norepinephrine did not stimulate phosphoinositide hydrolysis. Intracellular concentration of free Ca2+ ([Ca2+]i) was measured in Indo-1-loaded sympathetic neurons at rest and after addition of test agents. Measurements were made in the cell body and growth cone regions since Ca2+ mobilization is known to be different in different regions of the sympathetic neurons. ACh (nicotinic component was blocked by hexamethonium) and 5-HT failed to increase the [Ca2+]i, in the cell body as well as in the growth cone. The spontaneous release of [3H]-NE was not affected by ACh and 5-HT. Caffeine increased the [Ca2+]i only in the cell body but not in the growth cone and had no effect on the release of [3H]-NE. These results suggest that an IP3-insensitive but caffeine-sensitive pool of Ca2+ is present only in the somatic region of sympathetic neurons and is not coupled to the transmitter release.

Acetylcholine↗
PubMed1990

Effects of neurotransmitters and peptides on phospholipid hydrolysis in sympathetic and sensory neurons.

The effects of neurotransmitters and peptides on phosphoinositide hydrolysis were studied by measuring [3H]inositol monophosphate ([3H]IP) and protein kinase C (PKC) activity in the sympathetic and sensory neuronal cultures of the chick embryo. [3H]IP was increased in sympathetic neurons by acetylcholine (ACh), muscarine, serotonin (5-HT), and vasoactive intestinal polypeptide. ACh, muscarine, 5-HT, and bradykinin increased [3H]IP in sensory neuronal cultures. Dopamine, norepinephrine, histamine, and nerve growth factor did not stimulate [3H]IP formation in both cultures. ACh and phorbol 12,13-dibutyrate (PDB) increased the PKC activity by two- to sevenfold in the particulate fraction of both cultures. In sympathetic neurons, PKC activity was increased in the particulate fraction; activity in the cytosolic fraction was not affected. There was a 50% decline in the protein kinase C activity of the cytosolic fraction after PDB and ACh treatment of sensory cultures. The decline in PKC activity in the cytosolic fraction was attributed to the presence of nonneuronal cells in sensory cultures. To confirm this, the enzyme activity was determined in tissues that contain a heterogeneous population of cells. PDB activated PKC in the adrenal medulla and the brain of the rat. In both tissues there was a 65% decline in the PKC activity of the cytosolic fraction and about a 75% increase in the particulate fraction. We conclude that the mechanism of activation of protein kinase C in pure cultures of sympathetic neurons is different than in tissues containing a mixed population of neurons and nonneuronal cells.

Acetylcholine↗