Posted on 05/17/2006 10:24:44 PM PDT by neverdem
New research in specially bred mice has elucidated how the antidepressant Prozac works. Scientists have long known that in addition to discouraging synapses from reabsorbing the neurotransmitter serotonin, Prozac (known generically as fluoxetine) also increases the number of neurons (neurogenesis) in the adult brain. But exactly how the drug manages this multiplication trick has proved difficult to pin down. Now researchers have traced the development cascade of new neurons and determined where fluoxetine exerts its multiplying--and beneficial--effect.
Grigori Enikolopov at the Cold Spring Harbor Laboratory and his colleagues bred a new strain of mice that allowed them to track the development of mature neurons from stem cells using the different marker proteins expressed. Of the six stages of neuron development observed in this process, the scientists found that more than two weeks of fluoxetine treatment boosted the number of so-called amplifying neural progenitors (ANPs) by nearly 50 percent (a migratory stream of which is shown in the image above).
Subsequent testing in mice allowed to live for a month after fluoxetine treatment showed a similar increase in the overall number of neurons. "Together, these results suggest that the fluoxetine-induced increase in the number of ANP precursors in the [brain] later translates into an increase in the number of new neurons," the researchers write in the paper presenting the findings in the Proceedings of the National Academy of Sciences.
By isolating the step in neuron development that fluoxetine influences, the scientists have identified a new target for antidepressants that may have fewer side effects. The research also unveils the links in the chain leading from stem cells to new neurons as well as provides an animal tailor-made to investigate the mechanisms of other medicines and treatments, permitting a ray of hope into the darker regions of brain dysfunction.
del shannon knows...
Those must be some really happy mice on drugs (what, with all the experiments and the lab they are stuck in)
Interesting. Thanks!
I don't know, but my sister-in-law is weird, whether she's on Prozac or off...
Hope at last, my two surviving neurons might settle down and breed . . .
Microbes Convert Wastewater into Useable Electricity For anyone that's interested, I linked what I believe is the original, actual article on that thread.
FReepmail me if you want on or off my health and science ping list.
Cheers? What's the point of a monster size cartoon and screwing up the thread and comments display?
I forgive him... They are wearing Tarheels caps!!!
scarcasm
save
This is sort of an urban myth put forward by the Scientologists. Like all urban myths, it has anectdotal evidence to support it.
Some people on Prozac have committed suicide, true, but often people who are suffering from depression commit suicide. Virtually everyone being treated with Prozac has some form of depression. If Prozac had been shown to have a causal link with suicide, it would be off the market.
Of course, Tom Cruise would disagree with that, but he eats placenta...
Are you kidding? Have you seen the profit margin?
1: Pak J Pharm Sci. 1999 Jul;12(2):11-6. Related Articles, Links
Inhibition of rat liver tryptophan pyrrolase activity by fluoxetine.
Bano S, Morgan CJ, Badawy AA, Buckland PR, Guffin PM.
Cardiff Community Health Care NHS Trust, Biomedical Research Laboratory, Witchurch Hospital, Cardiff CF4 7XB, UK.
The present study has demonstrated the effectiveness of acute administration of fluoxetine to inhibit rat liver tryptophan pyrrolase activity. The maximum inhibition of basal liver tryptophan pyrrolase activity at 2 h after administration was observed with 1 mg/kg dose for the total enzyme and apoenzyme activities and that significant inhibition of these two activities was evident with a dose of the drug as small as 0.5 mg/kg. Serum free tryptophan concentrations were also increased using 10 mg/kg dose of fluoxetine. In view of the role of tryptophan depletion and thus 5-HT in pathophysiology of depression, it is strongly suggested that the inhibition of liver tryptophan pyrrolase activity may be a major mechanism of antidepressant action.
PMID: 16414828 [PubMed]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=search&DB=pubmed
I wonder if they ever take into account what impact this has on their little mice studies?
Who paid for this little smoke and mirrors study? I could never find it in the PDF doc.
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