Resumen:
K801 is a prototypical non-competitive NMDAreceptor-antagonist that induces behavioural changes andreversible toxicity at low doses, while at higher doses triggersneuronal death that mainly affects the retrosplenial cortex(RSC) and to a lesser extent other structures such asthe posterolateral cortical amygdaloid nucleus (PLCo). Themechanism of MK801-induced neurodegeneration remainspoorly understood. In this study we analysed the participationof GABA-ergic and glutamatergic neurotransmission inMK801-induced neuronal death. We used a single i.p. injectionof MK801 (2.5 mg/kg) that induced moderate neuronaldeath in the RSC and PLCo of female rats, and combined thistreatment with the i.p., i.c.v., or intra-RSC infusion of drugsthat are selective agonists or antagonists of the GABA-ergicor glutamatergic neurotransmission. We found that neuronaldeath in the RSC, but not the PLCo, was significantly redu