My mind raced for potential titles to a post when I read the recent report from Science, ‘The Antidepressant Fluoxetine Restores Plasticity in the Adult Visual Cortex,’ by a team headed by José Fernando Maya Vetencourt (abstract), but I’ve opted to be demure, rather than go with some of my other options (like ‘Anti-depressants the “Cocoon” pool for brain?’ or something similarly outrageous).
The research team investigated wither fluoxetine, a selective serotonin reuptake inhibitor (SSRI), could restore plasticity in the visual system of adult rats. They chose fluoxetine because long-term regimens of the drug promote neurogenesis and synaptogenesis in the hippocampus and increased activity of neurotrophin brain-derived neurotrophic factor (BDNF) and its primary receptor, TrkB (close paraphrase to the original article). These effects have been shown essential to the drug’s effect; block one of these processes, and the anti-depressant doesn’t work nearly as well. In order to test plasticity, the team studied how rats responded to monocular deprivation — covering one eye — both the initial shift in ocular dominance and then the recovery of visual function after long-term monocular deprivation. In general, the fluoxetine-treated rats responded in exaggerated fashion to both conditions, suggesting that plasticity was greater with long-term administration of the drug. From the abstract:
We found that chronic administration of fluoxetine reinstates ocular dominance plasticity in adulthood and promotes the recovery of visual functions in adult amblyopic animals, as tested electrophysiologically and behaviorally. These effects were accompanied by reduced intracortical inhibition and increased expression of brain-derived neurotrophic factor in the visual cortex. Cortical administration of diazepam prevented the effects induced by fluoxetine, indicating that the reduction of intracortical inhibition promotes visual cortical plasticity in the adult. Our results suggest a potential clinical application for fluoxetine in amblyopia as well as new mechanisms for the therapeutic effects of antidepressants and for the pathophysiology of mood disorders.
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