It is relatively less well known that much of the anti-depressant effect of medications like Prozac may be due to them leading to better neurogenesis in the brain/ hippocampus. It is more well known that depression may itself be caused due to reduced neurogenesis. What is most well known is the scientifically unproved ‘serotonin’ theory of depression and how SSRIs work by increasing the level of serotonin in the brain.

Now a new research paper shows that Prozac has a non-specific effect on plasticity ion the brain and can even be used to treat Ambylopia, a defect of visual system, by rewiring the brain. Here is the abstract:

We investigated whether fluoxetine, a widely prescribed medication for treatment of depression, restores neuronal plasticity in the adult visual system of the rat. 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.

Now this brings me to an important conclusion. We have shown earlier that depression is associated with a bland sense of taste and a bland sense of smell. I have also heard of anecdotal evidence (including from readers of this blog) that depression leads to loss of fine sensation capabilities in other realms too including loss of an ability to discern pitch. Thus, to me it seems that the reason one has bland sensations in depressive states may have to do with reduced neurogeneisis and loss of neurons in the sensory areas. Anti-depressants also restore the sense acuity back, so apparently they are able to induce neurogenisis and plasticity in other barin regions than the hippocampus and their anti-depressant effects may largely be due to this factor. I had hypothesized earlier that depressed people should have diminished sense in other areas too – like that of vision and it will be interesting to see if data exists to support this view. Are there disorders similar to the ‘lazy eye’ that are more common in depressed people than in normal controls ; if so they would definitely be cured by prozac and one reason why people may be getting better due to medication may be because they can feel the world as vivid again. I theorize that while everything seems more vivid in mania, the reverse is true for depression and the underlying reason may be the anomalous neurogenesis. If so, there is hope for people who get their senses diminished as a result of depression- with an insight into how anti-depressants work – by improving neurogenisis and plasticity- we may be able to make better drugs that benefit them.

I’ll be watching this anti-depressant as a general enhancer of plasticity theory very keenly in the future and would love any pointers to research on the same lines from my readers.

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