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Here, we have studied the involvement of neuroplasticity pathways and\/or the 5\u2010hydroxytryptaminergic system in the antidepressant\u2010like effect of this combined treatment, given subchronically.<\/jats:p><\/jats:sec><jats:sec><jats:title>EXPERIMENTAL APPROACH<\/jats:title><jats:p>Expression of brain\u2010derived neurotrophic factor (BDNF) and its receptor (TrkB), 5\u2010bromo\u20102\u2032\u2010deoxyuridine (BrdU) incorporation, and \u03b2\u2010catenin protein expression in different cellular fractions, as well as 5\u2010HT<jats:sub>1A<\/jats:sub> receptor function were measured in the hippocampus of rats treated with fluoxetine, ketanserin and fluoxetine + ketanserin for 7 days, followed by a forced swimming test (FST) to analyse antidepressant efficacy.<\/jats:p><\/jats:sec><jats:sec><jats:title>KEY RESULTS<\/jats:title><jats:p>mRNA for BDNF was increased in the CA3 field and dentate gyrus of the hippocampus by combined treatment with fluoxetine + ketanserin. Expression of \u03b2\u2010catenin was increased in total hippocampal homogenate and in the membrane fraction, but unchanged in the nuclear fraction after combined treatment with fluoxetine + ketanserin. These effects were paralleled by a decreased immobility time in the FST. There were no changes in BrdU incorporation, TrkB expression and 5\u2010HT<jats:sub>1A<\/jats:sub> receptor function in any of the groups studied.<\/jats:p><\/jats:sec><jats:sec><jats:title>CONCLUSIONS AND IMPLICATIONS<\/jats:title><jats:p>The antidepressant\u2010like effect induced by subchronic co\u2010treatment with a SSRI and a 5\u2010HT<jats:sub>2A<\/jats:sub> receptor antagonist may mainly be because of modifications in hippocampal neuroplasticity (BDNF and membrane\u2010associated \u03b2\u2010catenin), without a significant role for other mechanisms involved in chronic antidepressant response, such as hippocampal neuroproliferation or 5\u2010HT<jats:sub>1A<\/jats:sub> receptor desensitization in the dorsal raphe 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