Résumé
Although the epileptogenic properties of estrogens have been widely demonstrated in several models and species, the mechanism[s] by which estrogens can acutely change seizure parameters including after discharge and seizure duration remain remains to be determined. In the present study, we examined the role of NMDA [N-methyl-D-aspartate], non-NMDA and estrogenic receptors in estradiol benzoate [EB] effects on kindled seizure parameters. Different groups of fully kindled male rats received either EB [30 microg /kg]; EB plus MK801 [2 mg/kg, as NMDA antagonist]; DNQX [7.5 mg/kg]; tamoxifen [TAM, 0.1 mg/kg, as non-NMDA antagonist] or intra-amygdala injection of anisomycine [30 mmol/ml, a protein synthesis inhibitor]. Kindled seizure parameters including after discharge duration [ADD] and stage 5 duration [S5D] were determined at 0.25 and 3 h post sesame oil [EB solvent] or EB treatment. While pretreatment with either MK801 or DNQXcould block the ADD prolongation induced by EB at 0.25 h, they had no effect on S5D prolongation at 3 h. Moreover, application of anisomycine or TAM had no effect on estradiol induced ADD and S5D prolongation. These results indicate that both NMDA and non-NMD A receptors could be involved in EB induced ADD prolongation. The observed short term non-estrogenic receptor or protein synthesis dependent effects of EB may provide a non-genomic mechanism for the stimulatory effects of the steroid on seizure activity