Abstract
In mammalian CNS, GABAergic synaptic transmission (GABA = γ-aminobutyric acid) is fundamental to inhibitory feedback and feedforward circuits of projecting neurons and local interneurons. Up to 30% of all synapses in the brain are thought to be GABAergic. The synaptic inhibitory action of GABA is due to the opening of GABA-gated chloride channels, which in turn leads to an increase in the chloride conductance of the subsynaptic membrane. Most frequently, the chloride flux is directed inward, leading to a hyperpolarizing inhibitory postsynaptic potential. In recent years, studies of the GABAergic inhibitory synaptic transmission have unraveled a molecular mechanism by which anxiety, vigilance, muscle tension and the occurrence of convulsions can be regulated.
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© 1986 Springer-Verlag Berlin Heidelberg
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Möhler, H., Schoch, P., Richards, J.G. (1986). The GABA/Benzodiazepine Receptor Complex: Function, Structure and Location. In: Montalcini, R.L., Calissano, P., Kandel, E.R., Maggi, A. (eds) Molecular Aspects of Neurobiology. Proceedings in Life Sciences. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-70690-5_18
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DOI: https://doi.org/10.1007/978-3-642-70690-5_18
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