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The GABA Receptor-Chloride Ion Channel Protein Complex

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Neuroreceptors and Signal Transduction

Abstract

The majority of inhibitory synaptic transmission in the central nervous system involves γ-aminobutyric acid (GABA) as the neurotransmitter (1). The signal transduction mechanism at the majority of GABA synapses involves a ligand-gated chloride channel; binding of GABA to its receptor increases postsynaptic membrane chloride conductance and inhibits the target cell (2). This GABA receptor, called GABAA, is defined pharmacologically by sensitivity to the agonist muscimol anä the antagonist bicuculline (3). At least one other type of GABA receptor exists, GABAB, defined as insensitive to bicuculline and sensitive to baclofen; GKBAB receptors are coupled to GTP-binding proteins for a variety of signal transduction mechanisms (4). GABAA receptor function is also modulated by at least three classes of centrally active drugs, the picrotoxin-like convulsants, that inhibit GABA function, and the benzodiazepines and the barbiturates, both of which enhance GABA function (5).

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Olsen, R.W. et al. (1988). The GABA Receptor-Chloride Ion Channel Protein Complex. In: Kito, S., Segawa, T., Kuriyama, K., Tohyama, M., Olsen, R.W. (eds) Neuroreceptors and Signal Transduction. Advances in Experimental Medicine and Biology, vol 236. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-5971-6_1

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  • DOI: https://doi.org/10.1007/978-1-4757-5971-6_1

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