Abstract
It is generally assumed that the synaptic inhibition in adult hippocampus is mediated by GABA, which acts on GABA-A (Ben-Ari and al 1981, Alger and Nicoll 1982, Kehl and Mc Lennan 1985), and GABA-B receptors, coupled to chloride and potassium channels respectively (Alger-and Nicoll 1982, Dutar and Nicoll 1988). When the inhibition is blocked by GABAergic antagonist, interictal discharges, mediated by excitatory amino acids appear (Wong and Traub 1983, Neuman and al 1988 b). Extensive theorical and experimental data indicate that the well known propensity of CA3 neurons to generate synchronized burst is due to the presence of recurrent excitatory collateral’s between pyramidal neurons (Mc Vicar and Dudeck 1980, Wong and Traub 1983, Miles and Wong 1986).
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Gaïarsa, J.L., Corradetti, R., Ben-Ari, Y., Cherubini, E. (1990). GABA Mediated Synaptic Events in Neonatal Rat CA3 Pyramidal Neurons in Vitro: Modulation by NMDA and Non-NMDA Receptors. 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_18
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DOI: https://doi.org/10.1007/978-1-4684-5769-8_18
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