On the mechanism by which veratridine causes a calcium-independent release of gamma-aminobutyric acid from brain slices

British Journal of Pharmacology
J Cunningham, M J Neal

Abstract

1 The mechanisms by which veratridine increases the release of gamma-aminobutyric acid (GABA) from brain slices have been studied.2 Exposure of superfused cerebro-cortical, nigral or cerebellar slices to veratridine (5 muM) or KCl (50 mM) caused large increases in the efflux of [(3)H]-GABA.3 Reduction of the external Ca concentration [Ca](o) to zero had strikingly different effects on the veratridine and K-evoked release of [(3)H]-GABA. The K-evoked release from all three areas was greatly reduced in Ca-free medium, but the veratridine-evoked release from cerebeller slices was not affected, and the release of [(3)H]-GABA from cortical and nigral slices was increased three fold. The potentiation of the veratridine evoked release of GABA which occurred in Ca-free medium was not due to the reduction in divalent ions, because it still occurred in medium in which the Ca was replaced by an equivalent amount of Mg.4 The veratridine-evoked release of [(14)C]-glycine from slices of spinal cord was also significantly increased in Ca-free medium. In contrast, the release of cortical [(3)H]-noradrenaline and [(14)C]-acetylcholine caused by the alkaloid was greatly diminished in Ca-free medium.5 The veratridine but not the K-evoked release ...Continue Reading

References

Aug 1, 1977·Journal of Neurochemistry·J S De Belleroche, H F Bradford
Oct 1, 1974·Physiological Reviews·T Narahashi
Jan 22, 1971·Biochemical and Biophysical Research Communications·C L Moore
May 1, 1974·The Biochemical Journal·K C Reed, F L Bygrave
Aug 1, 1972·Proceedings of the National Academy of Sciences of the United States of America·M P BlausteinP Needleman
May 1, 1971·The Journal of Physiology·M J Neal
Feb 1, 1968·The Journal of General Physiology·B Hille
Oct 1, 1968·Journal of Neurochemistry·L L Iversen, M J Neal
Jul 11, 1957·The Journal of Physiology·B FRANKENHAEUSER, A L HODGKIN

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Citations

Jun 1, 1984·Pflügers Archiv : European journal of physiology·N BernardiN Davidson
Jan 1, 1993·Journal of Neural Transmission. General Section·A GalliL Coppini
Jan 1, 1984·Journal of Neural Transmission·J A HardyP R Dodd
Nov 4, 1986·European Journal of Pharmacology·S L ErdöL Szporny
May 12, 1995·Mechanisms of Ageing and Development·D DobrevK Andreas
Jan 1, 1989·Neurochemistry International·S BernathM J Zigmond
Jan 1, 1990·Neurochemistry International·P P GonçalvesA P Carvalho
Jan 1, 1989·Progress in Neurobiology·R J Huxtable
Jan 1, 1986·Comparative Biochemistry and Physiology. C, Comparative Pharmacology and Toxicology·J D DohertyN Salem
Jan 1, 1985·Neuroscience Research. Supplement : the Official Journal of the Japan Neuroscience Society·S Yazulla
Feb 1, 1991·Acta Physiologica Scandinavica·M Pérez de la MoraK Fuxe
Jan 30, 2016·Journal of Neurochemistry·Michael P RassnerThomas J Feuerstein
Apr 1, 1983·Human Toxicology·P CarlierE Fournier
Jan 1, 1987·Journal of Neuroscience Research·S S Oja, P Kontro
Oct 15, 2013·The European Journal of Neuroscience·Petr UnichenkoSergei Kirischuk
Aug 1, 1986·Journal of Neurochemistry·J P PinJ Bockaert

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