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GABA-Activated Bicarbonate Conductance

Influence on EGABA and on Postsynaptic pH Regulation

  • Chapter
Chloride Channels and Carriers in Nerve, Muscle, and Glial Cells

Abstract

γ-Aminobutyric acid (GABA) is a transmitter compound with a wide distribution and an exclusively inhibitory role in both vertebrate and invertebrate nervous systems (Gerschenfeld, 1973; Krnjević, 1974). Apart from its action on vertebrate GABAB-type receptors (see Dutar and Nicoll, 1988), the inhibitory effect of GABA is based on the opening of postsynaptic Cl channels (Boistel and Fatt, 1958; Siggins and Gruol, 1986). An increase in postsynaptic Cl conductance is also characteristic of glycine-mediated inhibition in vertebrates (Siggins and Gruol, 1986) and of acetylcholine-mediated inhibition in some invertebrate synapses (e.g., Kerkut and Thomas, 1964). The inhibitory effect of an increase in postsynaptic Cl conductance is due to the fact that in most excitable cells, the equilibrium potential of chloride is at a level more negative than the threshold for action-potential generation.

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Kaila, K., Voipio, J. (1990). GABA-Activated Bicarbonate Conductance. In: Alvarez-Leefmans, F.J., Russell, J.M. (eds) Chloride Channels and Carriers in Nerve, Muscle, and Glial Cells. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-9685-8_12

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