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Title: Membrane events and ionic processes involved in dopamine release from tuberoinfundibular neurons. II. Effect of the inhibition of the Na+-Ca++ exchange by amiloride

In the present study we investigated the effect of amiloride, a rather specific inhibitor of the membrane Na+-Ca++ exchange system, on the release of endogenous dopamine (DA) and previously taken-up (3H)DA from tuberoinfundibular dopaminergic neurons. Amiloride (300 microM) stimulated either endogenous DA or (3H)DA release. Amiloride-induced stimulation of (3H)DA release was prevented in a Ca++-free plus ethylene glycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid medium. Amiloride, at the same concentration, reinforced both high K+- and electrically-induced stimulation of (3H)DA release. These results are explained on the basis of the ability of amiloride in blocking the Na+-Ca++ exchange system, therefore causing an elevation of intracellular Ca++ levels in resting conditions, and a further accumulation of Ca++ ions after high K+- or electrically elicited opening of voltage-operated channels specific for Ca++ ions. The enhanced intracellular Ca++ availability may trigger the stimulation of neurotransmitter release. In addition, amiloride was able to block in a dose-dependent manner (70-300 microM) the ouabain-induced (3H)DA release, suggesting that, when intracellular concentrations of Na+ are increased by the blockade of Na+,K+-adenosine triphosphatase the Na+-Ca+;+ exchange carrier reverses its resting mode of operation, mediating the influx of extracellular Ca++ ions. Amiloride, by blocking the Na+-Ca++ exchange mechanism, prevents the ouabain-elicited entrance ofmore » extracellular Ca++ ions, therefore inhibiting (3H)DA release stimulated by the cardioactive glycoside. Collectively, the results of the present study seem to be compatible with the idea that the Na+-Ca++ exchange mechanism is involved in the regulation of (3H)DA release from tuberoinfundibular dopaminergic neurons, through the regulation of Ca++ movements across the plasma membrane.« less
Authors:
; ; ; ;
Publication Date:
OSTI Identifier:
6805328
Resource Type:
Journal Article
Resource Relation:
Journal Name: J. Pharmacol. Exp. Ther.; (United States); Journal Volume: 246:2
Research Org:
Unive. of Naples (Italy)
Country of Publication:
United States
Language:
English
Subject:
59 BASIC BIOLOGICAL SCIENCES; CALCIUM COMPOUNDS; MEMBRANE TRANSPORT; DIURETICS; BIOLOGICAL EFFECTS; DOPAMINE; SECRETION; SODIUM COMPOUNDS; ATP-ASE; CATIONS; CELL MEMBRANES; HYPOTHALAMUS; IN VITRO; INHIBITION; ION EXCHANGE; OUABAIN; RATS; TRACER TECHNIQUES; TRITIUM COMPOUNDS; ACID ANHYDRASES; ALKALI METAL COMPOUNDS; ALKALINE EARTH METAL COMPOUNDS; AMINES; ANIMALS; AROMATICS; AUTONOMIC NERVOUS SYSTEM AGENTS; BODY; BRAIN; CARBOHYDRATES; CARDIAC GLYCOSIDES; CARDIOTONICS; CARDIOVASCULAR AGENTS; CELL CONSTITUENTS; CENTRAL NERVOUS SYSTEM; CHARGED PARTICLES; DRUGS; ENZYMES; GLYCOSIDES; HYDROLASES; HYDROXY COMPOUNDS; IONS; ISOTOPE APPLICATIONS; LABELLED COMPOUNDS; MAMMALS; MEMBRANES; NERVOUS SYSTEM; NEUROREGULATORS; ORGANIC COMPOUNDS; ORGANS; PHENOLS; PHOSPHOHYDROLASES; POLYPHENOLS; RODENTS; STROPHANTHINS; SYMPATHOMIMETICS; VERTEBRATES 550201* -- Biochemistry-- Tracer Techniques