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Effects of lamotrigine on behavior, oxidative parameters and signaling cascades in rats exposed to the chronic mild stress model

► Effects of lamotrigine in rats exposed to stress. ► Lamotrigine reversed anhedonia in stressed rats. ► Lamotrigine decreased oxidative damage in the rat brain. ► Lamotrigine increased antioxidant enzymes in the rat brain. The rats were subjected to 40 days of stress protocol, during which the sucr...

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Published in:Neuroscience research 2013-04, Vol.75 (4), p.324-330
Main Authors: Abelaira, Helena M., Réus, Gislaine Z., Ribeiro, Karine F., Steckert, Amanda V., Mina, Francielle, Rosa, Daniela V.F., Santana, Cíntia V., Romano-Silva, Marco Aurélio, Dal-Pizzol, Felipe, Quevedo, João
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Language:English
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Summary:► Effects of lamotrigine in rats exposed to stress. ► Lamotrigine reversed anhedonia in stressed rats. ► Lamotrigine decreased oxidative damage in the rat brain. ► Lamotrigine increased antioxidant enzymes in the rat brain. The rats were subjected to 40 days of stress protocol, during which the sucrose consumption was assessed in rats chronically treated with lamotrigine (20mg/kg) or with saline. The signaling cascade and oxidative stress parameters were assessed in the brain rat. Both control and stressed rats treated with lamotrigine showed an increase on malondialdehyde equivalents (MDA) in the prefrontal cortex, and that there was also an increase in the amygdala of the control rats treated with lamotrigine. The carbonyl protein was increased in the prefrontal cortex of the stressed group treated with saline, however, the lamotrigine treatment reversed this effect. The treatment with lamotrigine increased the superoxide dismutase (SOD) and catalase activity (CAT) activities in the amygdala of stressed rats. The protein kinase B (PKB/Akt) was reduced in the amygdala in the stressed group treated with saline or lamotrigine. We suggest that the antidepressant-like effect of lamotrigine on anhedonic behavior may be related at least in part to its effects on the oxidative stress parameters and AKT.
ISSN:0168-0102
1872-8111
DOI:10.1016/j.neures.2013.02.002