Fluoxetine treatment is often associated with an increase in BDNF (Brain-derived neurotrophic factor), a protein which encourages the development of new synapses in the brain areas responsible for higher-order thinking and other functions. At first glance this sounds great, as the Scientific American authors concluded. However, other researches, such as those in the study I linked above, hypothesize that this increase in BDNF and neuronal growth may actually be due to neuronal insult from fluoxetine. In other words, the increase in plasticity and new cell growth might be a healing response from the brain following damage caused by fluoxetine.
Furthermore, fluoxetine is an older SSRI with effects and receptor affinities that extend beyond the serotonin system. When using fluoxetine for research, caution must be taken to separate the effects on the serotonin system from the effects of other functions of fluoxetine. Without further study, we can't know if these effects apply to all SSRIs, or just fluoxetine.
I should also note: All of this is great for future R&D of next-generation anti-depressants, but it should not be used by anyone when determining a treatment path. Despite the study I linked above, to my knowledge we haven't seen any deleterious effects on memory or cognition due to SSRI treatment in the general population. The bottom line is that we don't know why or how SSRIs work (despite what the drug company marketing department wants you to believe), but they are effective for many people. And combined with therapy, the rate of remission improves even more.
"Previously, researches have found that fluoxetine (Prozac) actually suppresses neuronal growth in vitro"
Neurogenesis is only one type of plasticity, and it doesn't sound like the type they're talking about in this article. (Albeit I didn't read the study.)
While they didn't measure neurogenesis directly in the study, they did measure BDNF (Brain-derived neurotrophic factor) which can induce neuron growth[1]. Essentially they took two groups of mice: regular mice, and mice whose BDNF levels are believed to not respond to Prozac (Flx). They found that in regular mice, Prozac plus retraining reduced anxiety. In those mice in which Prozac doesn't increase BDNF, the Prozac effect went away.[2]
I know it's hard to read the actual study all the time, but sometimes it helps. :)
[2]Because mice heterozygous for the BDNF null allele (BDNF+/−) are insensitive to Flx treatment in behavioral models of depression and anxiety (3, 26), we tested whether BDNF+/− mice (C57Bl/6J background) responded differentially to Flx in the fear-conditioning paradigm. Flx again prevented fear renewal in the wild-type mice, but in BDNF+/− littermates trained to fully extinguish the fear response, the Flx effect was absent as indicated by elevated levels of freezing 1 week after extinction (Fig. 4B and fig. S7). To test whether BDNF was acting predominately in the amygdala, we used doxycycline-regulatable lentiviral infection to overexpress BDNF locally in the BLA from the end of extinction onward (figs. S8 and S9). BDNF-overexpressing mice did not show fear renewal, whereas control mice did (Fig. 4C).
Previously, researches have found that fluoxetine (Prozac) actually suppresses neuronal growth in vitro:
http://www.ncbi.nlm.nih.gov/pubmed/20377614
Fluoxetine treatment is often associated with an increase in BDNF (Brain-derived neurotrophic factor), a protein which encourages the development of new synapses in the brain areas responsible for higher-order thinking and other functions. At first glance this sounds great, as the Scientific American authors concluded. However, other researches, such as those in the study I linked above, hypothesize that this increase in BDNF and neuronal growth may actually be due to neuronal insult from fluoxetine. In other words, the increase in plasticity and new cell growth might be a healing response from the brain following damage caused by fluoxetine.
Furthermore, fluoxetine is an older SSRI with effects and receptor affinities that extend beyond the serotonin system. When using fluoxetine for research, caution must be taken to separate the effects on the serotonin system from the effects of other functions of fluoxetine. Without further study, we can't know if these effects apply to all SSRIs, or just fluoxetine.
I should also note: All of this is great for future R&D of next-generation anti-depressants, but it should not be used by anyone when determining a treatment path. Despite the study I linked above, to my knowledge we haven't seen any deleterious effects on memory or cognition due to SSRI treatment in the general population. The bottom line is that we don't know why or how SSRIs work (despite what the drug company marketing department wants you to believe), but they are effective for many people. And combined with therapy, the rate of remission improves even more.