Abstracts

Early life stress has enduring behavioral and neuroendocrine effects, particularly affecting the hippocampus and amygdala. This may be relevant to temporal lobe epilepsy (TLE) - an epileptoform in which these limbic brain structures are strongly implicated. In rats, we tested the hypothesis that early postnatal stress, in the form of maternal separation, creates vulnerability to limbic epileptogenesis in adult life., On postnatal days 2-14, we employed either maternal separation for 180 min/day (HMS180, n=18) or brief neonatal handling (15 min/day; HMS15, n=18) to mixed gender Non-Epileptic Control (NEC) rats. At 7 weeks of age, both groups were implanted with bipolar electrodes into the left amygdala and one week later, rapid amygdala kindling commenced (RAK - 10 sec bursts of 400[mu]A every 15 mins, 24 times per day). Kindling continued for up to 120 stimulations until subjects were deemed to be fully-kindled (five class V seizures - Racine scale). Rats were then survived for a futher 2 weeks prior to histological analysis., Fewer stimulations were required in the HMS180 group than in the HMS15 group to reach the fully kindled state (44.4 [plusmn] 3.7, n = 18 vs. 72.0 [plusmn] 7.8, n = 18; [italic]p[/italic] [lt] 0.01). Repeated measures ANOVA revealed significant differences: (i) between treatment groups ([italic]p[/italic] [lt] 0.01), (ii) over time as seizures progressed ([italic]p[/italic] [lt] 0.001), and (iii) between treatment groups, over time ([italic]p[/italic] = [lt]0.001).[figure1], This study demonstrates that postnatal maternal separation stress results in persisting vulnerability to limbic epileptogenesis. This has implications for human TLE and its psychiatric co-morbidities, suggesting a common causation model., (Supported by an NHMRC project grant (400088), and a NARSAD Independent Investigator Award (TOB).)