CNS neuroscience & therapeutics · 2017
Prenatal alcohol exposure enhances the susceptibility to NMDA-induced generalized tonic-clonic seizures in developing rats.
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Cho Sue J, Lovinger David M, N'Gouemo Prosper
Аннотация
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, while WRS, GTCS, and TS were observed 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.
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, while WRS, GTCS, and TS were observed 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.