Published: May 19, 2009
For many years, selective serotonin reuptake inhibitors (SSRIs) such as prozac have been a favorite pharmalogical treatment for depression. Interestingly, it is often weeks before the psychological effects of these drugs kick in, the cause of this lag period being largely unknown. As the drug is known to increase neurogenesis, some believe this upregulation of newborn cells - and the gradual time it takes for this process to occur - underlies the delayed impact of SSRIs.
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In a "recent" study published in Science magazine, Vetencourt et al throw another interpretation into the hat. Their study indicates that under the influence of fluoxetine (aka prozac), the adult rat visual cortex can undergo levels of reorganization typically restricted to developmental periods of life. This enhanced plasticity appears to be mediated by a decrease in inhibitory GABAergic signaling (an increase in which is known to coincide with the end of the critical period during development). The authors ostensibly focus on how fluoxetine can be used as a treatment for amblyopia, a condition where signaling from one eye is impaired due to input deprivation during development. However, considering many systems-level plastic changes often take weeks to emerge in adult animals, one immediately wonders if reorganization of particular emotional areas of the brain might underlie the mood-enhancing effects of SSRIs (and, if so, why are such effects unipolar in their psychological consequence?). Or perhaps it is an overabundance of inhibitory signaling that SSRIs rectify? Whatever the case, given what we already know about plasticity and sensory processing, you might consider increasing your vitamin p intake next time you take on a new language (I hear the side effects are pretty tolerable).
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