Abstract
In the mammalian cortex, glutamate (1) amd γ-aminobutyric acid (GABA) (2) are the principal transmitters mediating excitatory and inhibitory synaptic events. Glutamate activates cation conductances that lead to membrane depolarization. This action is mediated by at least three distinct receptor subtypes defined by their main agonists as N-methyl-D-aspartate (NMDA), quisqualate and kainate receptors (1). GABA controls at least two conductances that produce hyperpolarization in cortical neurons: an early inhibitory synaptic potential mediated by chloride currents through GABAA receptors (2) and a late hyperpolarization mediated by potassium current through GABAB receptors (3).
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Stelzer, A. (1990). Regulation of GABAA Currents by Excitatory Amino Acids. In: Ben-Ari, Y. (eds) Excitatory Amino Acids and Neuronal Plasticity. Advances in Experimental Medicine and Biology, vol 268. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5769-8_29
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DOI: https://doi.org/10.1007/978-1-4684-5769-8_29
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