Anti-Excitotoxic Actions of Taurine in the Rat Hippocampus Studied in Vivo and in Vitro

Abstract

The role of neuroactive amino acids in seizure phenomena has been a subject of intensive study in the past (Morselli et al., 1981; Perry and Hansen, 1981; Huxtable et al., 1983). An additional impetus to this area of research followed the observation that exogenous excitatory amino acids, such as kainic acid, can produce in animals an electroencephalographic and neuropathological profile reminiscent of that found in human patients with temporal lobe epilepsy (Nadler et al., 1978; Pisa et al., 1980; Lothman and Collins, 1981; Sloviter and Damiano, 1981; French et al., 1982; Ben-Ari, 1985). Thus, it was reasonable to conclude that endogenous excitatory amino acids bearing structural similarities to kainate might play pivotal roles in the etiology of seizure disorders. In this regard, glutamate, aspartate, and, more recently, quinolinate (QUIN), endogenous excitants of central nervous tissue, have been suggested as factors involved in initiating events leading to seizures (Lapin, 1978; Coutinho-Netto et al., 1981; Nitsch et al., 1983; Smialowski, 1983; Schwarcz et al., 1984). This conjecture has been indirectly validated by the recent observations that excitatory amino acid antagonists possess anticonvulsant activity in a number of animal models of epilepsy (Croucher et al., 1982; Meldrum et al., 1983; Schwarcz et al., 1984).