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5-HT and antidepressants: new views from microdialysis studies

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    A study reported reduced social interactions in rats treated with fluoxetine (10 mg/kg, IP daily), observed 4, 7, and 14 days post-treatment, were resolved after treatment for 28 days (Bristow et al. 2000). However, chronic SSRI treatment produced excess extracellular 5-HT, leading to higher postsynaptic receptor activation than in acute treatment (Artigas, 1993). Recently, it has been shown that exposure to fluoxetine from the prenatal stage to adulthood can impair social novelty recognition in adult males (Yu et al. 2019).

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    This model, however, falls short in explaining several physiological and clinical observations such as the common failure of antidepressant drugs or the beneficial, long-term improvements observed in neuronal plasticity of DRN 5-HT neurons during the antidepressant response as exemplified with the multimodal antidepressant vortioxetine: rapid recovery (3 days) of 5-HT firing (Betry et al., 2013) but a still delayed onset (1 month) of antidepressant response (Orsolini et al., 2017). Artigas (1993) first hypothesized that blocking the 5-HT1A autoreceptor could prevent the negative feedback observed after chronic SSRI treatment, thus increasing 5-HT release in cortical and limbic areas, and reduce the delay of action of those treatments. Preclinical studies confirmed this hypothesis: rats with a combination of citalopram and 5-HT1 receptor antagonist (S)-UH-301 had a higher level of extracellular 5-HT in the hippocampus, than those who received citalopram alone (Hjorth 1993).

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