These findings suggest that the TRPV1 channel is a promising molecular target for seizure suppression, with female GEPR-3s exhibiting higher sensitivity than male GEPR-3s.

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Aims Prenatal alcohol exposure (PAE) is associated with a higher likelihood of developing generalized tonic-clonic seizures (GTCS) in infants and children. However, experimental studies of PAE-related seizures have yielded conflicting results. Here, we investigated the effect of acute PAE on N-methyl-D-aspartate (NMDA)-induced seizures in developing rats. Methods Pregnant Sprague-Dawley rats were given an oral dose of either ethanol (5 g/kg body weight) or vehicle on embryonic day 18. The offspring were tested for susceptibility to NMDA-induced seizures on postnatal day 7 (P7), 21 (P21), 35 (P35) and 42 (P42). Specifically, the prevalence and latency of NMDA-induced continuous wild running-like behaviors (CWR), flexion seizures (FS), wild running seizures (WRS), GTCS, and tonic seizures (TS) were recorded and analyzed. Results N-methyl-D-aspartate-induced seizures consisted of CWR, FS, GTCS and TS in P21 rats. Thus, GTCS were consistently observed during development. PAE significantly increases the prevalence of GTCS in female and male P7-P21 rats and P7-P35 rats, respectively, but not in older rats. PAE also increases the prevalence of TS in male, but not female P21-P35 rats. Conclusions The PAE animal model of GTCS may provide a new opportunity to investigate the mechanisms that underlie neuronal hyperexcitability in developing animals prenatally-exposed to alcohol.

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