Various stresses affect neuronal functions, including the onset and progression of seizures, in animals and humans of all ages. However, the effect of stress on the convulsion in juvenile animals has been rarely investigated. In the present study, we investigated the effect of swim stress on the convulsion threshold in juvenile and adult mice, and the involvement of brain monoaminergic systems in establishing this threshold. In the pentylenetetrazol-induced convulsion model, acute swim stress increased the convulsion threshold in adult mice, whereas repeated swim stress increased it in both juvenile and adult mice. Microdialysis study showed that in the medial prefrontal cortex (mPFC) of juvenile mice, repeated swim stress caused lasting elevation of dopamine (DA) release relative to the basal levels. In contrast, acute swim stress increased noradrenaline release from the mPFC of both juvenile and adult mice compared with the basal levels; the elevation was higher in adult mice. Pretreatment with SCH23390 or haloperidol at low doses suppressed the anticonvulsant effect by repeated swim stress in juvenile mice. Yohimbine clearly abolished the anticonvulsant effect by acute swim stress in adult mice. These results indicated a critical role of brain monoamine in establishing the convulsion threshold. Also, DA system in the mPFC may play an important role in the anticonvulsant effects of repeated swim stress in juvenile mice.
Brain research 07/2012; 1473:104-13. DOI:10.1016/j.brainres.2012.07.031 · 2.83 Impact Factor