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The GABA Receptor/Benzodiazepine Complex in the Central Nervous System

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Neurobiochemistry

Abstract

One of the governing principles of neuronal communication in the central nervous system is the integration of neuronal excitation and inhibition. Various neurotransmitters, such as glutamate, aspartate, and certain neuropeptides, are able to stimulate neuronal activity. Inhibition of neuronal activity is exerted mainly by neurons operating with the neurotransmitter γ-aminobutyrate (GABA). Up to 30% of all synapses in the brain are thought to be GABAergic. They operate mainly in inhibitory feedback and feedforward circuits provided by GABAergic projecting neurons and local GABAergic interneurons (Roberts 1984). The synaptic inhibitory action of GABA is due to the opening of GABA-gated chloride channels leading to an increase in the chloride conductance of the subsynaptic membrane (Krnjevic 1976, Werman 1979, Peck 1980, Hamill et al. 1983, Simmonds 1984). Most frequently, the chloride flux is directed inward, leading to an inhibitory postsynaptic potential. Thereby, the excitability of the effector neuron is reduced.

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© 1985 Springer-Verlag Berlin Heidelberg

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Möhler, H., Schoch, P., Richards, J.G. (1985). The GABA Receptor/Benzodiazepine Complex in the Central Nervous System. In: Hamprecht, B., Neuhoff, V. (eds) Neurobiochemistry. Colloquium der Gesellschaft für Biologische Chemie 18.–20. April 1985 in Mosbach/Baden, vol 36. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-70940-1_14

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  • DOI: https://doi.org/10.1007/978-3-642-70940-1_14

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-70942-5

  • Online ISBN: 978-3-642-70940-1

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