Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Membrane electrical properties and the response to somatostatin were examined in dissociated human pituitary adenoma cells that secrete growth hormone (GH). Under current clamp condition with a patch electrode, the resting potential was -52.4 +/- 8.0 mV, and spontaneous action potentials were observed in 58% of the cells. Under voltage clamp condition an outward K+ current, a tetrodotoxin-sensitive Na+ current, and a Ca2+ current were observed. Cobalt ions suppressed the Ca2+ current. The threshold of Ca2+ current activation was about -60 mV. Somatostatin elicited a membrane hyperpolarization associated with increased membrane permeability in these cells. The reversal potential of somatostatin-induced hyperpolarization was -78.4 +/- 4.3 mV in 6 mM K+ medium and -97.2 +/- 6.4 mV in 3 mM K+ medium. These reversal potential values and a shift with the external K+ concentration indicated that membrane hyperpolarization was caused by increased permeability to K+. The hyperpolarized membrane potential induced by somatostatin was -63.6 +/- 5.9 mV in the standard medium. This level was subthreshold for Ca2+ and Na+ currents and was sufficient to inhibit spontaneous action potentials. Hormone secretion was significantly suppressed by somatostatin and cobalt ions. Therefore, we suggest that Ca2+ entering the cell through voltage-dependent channels are playing an important role for GH secretion and that somatostatin suppresses GH secretion by blocking Ca2+ currents. Finally, we discuss other possibilities for the inhibitory effect of somatostatin on GH secretion.
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PMID:Hyperpolarization of the membrane potential caused by somatostatin in dissociated human pituitary adenoma cells that secrete growth hormone. 287 59

Regulation of somatostatin (SS) secretion was studied in an in vitro system using collagenase-dispersed cells from fetal rat hypothalamus maintained in long term monolayer culture. Cultured cells exhibit a measurable basal secretion of immunoactive SS (SSLI) which can be augmented by carbachol, acetylcholine, or oxotremorine. The EC50 for carbachol is about 1 microM. Atropine, but not hexamethonium, antagonizes the action of cholinergic agonists. Cobalt or tetrodotoxin pretreatment diminishes basal secretion and eliminates the response to carbachol. Serotonin, several serotonin agonists, and gamma-aminobutyric acid (GABA) suppress carbachol-induced secretion. The GABA blockers bicuculline or picrotoxinin reverse the effect of added GABA and by themselves also augment SSLI secretion. Picrotin is inactive. The direct response to either bicuiculline or picrotoxinin is prevented by cobalt or tetrodotoxin treatment. These observations are consistent with the presence of a muscarinic cholinergic receptor which acts by a mechanism depending on an action potential and calcium influx to enhance the release of SSLI from neurosecretory cells. The data also support the conclusion that GABAergic transmission occurs within the cultures to tonically inhibit SSLI secretion. GABAergic, cholinergic, and serotoninergic systems may thus interact at the level of the hypothalamus to modulate SS secretion in vivo and thereby influence anterior pituitary release of GH and TSH.
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PMID:Muscarinic cholinergic stimulation of somatostatin secretion from long term dispersed cell cultures of fetal rat hypothalamus: inhibition by gamma-aminobutyric acid and serotonin. 612 32