QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Voipio, J Articles by Kaila, K Search for Related Content PubMed Articles by Voipio, J Articles by Kaila, K

Journal of Experimental Biology, Vol 156, Issue 1 349-360, Copyright © 1991 by Company of Biologists

JOURNAL ARTICLES

Effect of gamma-aminobutyric acid on intracellular pH in the crayfish stretch-receptor neurone

J Voipio, M Pasternack, B Rydqvist and K Kaila
Department of Zoology, University of Helsinki, Finland.

The effect of gamma-aminobutyric acid (GABA) on intracellular pH (pHi) was examined in the crayfish stretch-receptor neurone using H(+)-selective microelectrodes and a two-microelectrode voltage clamp. In the presence of 30 mmol l-1 HCO3- (pH 7.4), application of GABA (0.5 mmol l-1) produced a mean fall in pHi of 0.26 units. The initial rate of fall of pHi was attributable to a net influx of acid equivalents of 6.3 mmol l-1 min-1. In the nominal absence of HCO3-, GABA had little effect on pHi. The HCO3(-)-dependent acidosis caused by GABA was inhibited by picrotoxin (0.1 mmol l-1) but not by depletion of extracellular and intracellular Cl-. Acetazolamide (0.1 mmol l-1) decreased the rate of fall of pHi caused by a step increase in CO2 partial pressure as well as by GABA, which indicates that the neurone contains carbonic anhydrase. In the presence of both Cl- and HCO3-, the reversal potential of the GABA-activated current was more positive than under nominally HCO3(-)-free conditions. In line with this, GABA induced a marked HCO3(-)-dependent depolarization, and this depolarizing action was enhanced in the absence of Cl- so as to lead to triggering of action potentials. All these observations support the conclusion that the GABA-induced fall in pHi is due to a net efflux of HCO3- through the inhibitory anion channels.

This article has been cited by other articles:

				Y. Ben-Ari, J.-L. Gaiarsa, R. Tyzio, and R. Khazipov GABA: A Pioneer Transmitter That Excites Immature Neurons and Generates Primitive Oscillations Physiol Rev, October 1, 2007; 87(4): 1215 - 1284. [Abstract] [Full Text] [PDF]

				C. Rivera, J. Voipio, and K. Kaila Two developmental switches in GABAergic signalling: the K+-Cl- cotransporter KCC2 and carbonic anhydrase CAVII J. Physiol., January 1, 2005; 562(1): 27 - 36. [Abstract] [Full Text] [PDF]

				M. CHESLER Regulation and Modulation of pH in the Brain Physiol Rev, October 1, 2003; 83(4): 1183 - 1221. [Abstract] [Full Text] [PDF]

				S. Smirnov, P. Paalasmaa, M. Uusisaari, J. Voipio, and K. Kaila Pharmacological Isolation of the Synaptic and Nonsynaptic Components of the GABA-Mediated Biphasic Response in Rat CA1 Hippocampal Pyramidal Cells J. Neurosci., November 1, 1999; 19(21): 9252 - 9260. [Abstract] [Full Text] [PDF]

				L. Kiss and S. J. Korn Modulation of N-Type Ca2+ Channels by Intracellular pH in Chick Sensory Neurons J Neurophysiol, April 1, 1999; 81(4): 1839 - 1847. [Abstract] [Full Text] [PDF]

				M. Luckermann, S. Trapp, and K. Ballanyi GABA- and Glycine-Mediated Fall of Intracellular pH in Rat Medullary Neurons In Situ J Neurophysiol, April 1, 1997; 77(4): 1844 - 1852. [Abstract] [Full Text] [PDF]