Here's another article that I like: http://www.nature.com/mp/journal/v5/n3/abs/4000712a.html Here's the abstract:
*Neurogenesis (the birth of new neurons) continues postnatally and into adulthood in the brains of many animal species, including humans. This is particularly prominent in the dentate gyrus of the hippocampal formation. One of the factors that potently suppresses adult neurogenesis is stress, probably due to increased glucocorticoid release. Complementing this, we have recently found that increasing brain levels of serotonin enhance the basal rate of dentate gyrus neurogenesis. These and other data have led us to propose the following theory regarding clinical depression. Stress-induced decreases in dentate gyrus neurogenesis are an important causal factor in precipitating episodes of depression. Reciprocally, therapeutic interventions for depression that increase serotonergic neurotransmission act at least in part by augmenting dentate gyrus neurogenesis and thereby promoting recovery from depression. Thus, we hypothesize that the waning and waxing of neurogenesis in the hippocampal formation are important causal factors, respectively, in the precipitation of, and recovery from, episodes of clinical depression. **Molecular Psychiatry*(2000) *5,* 262-269. Carol On Mon, Nov 26, 2012 at 10:34 AM, Mike Palij <[email protected]> wrote: > To add to what David says below, the journal "Philosophical Transactions > of the Royal Society-B (Biological Sciences) recently had a special issue > on > the "serotonin hypothesis" (NOTE: it is important to note that it is a > hypothesis > and not just a description) which can be accessed here: > http://rstb.**royalsocietypublishing.org/**content/367/1601.toc<http://rstb.royalsocietypublishing.org/content/367/1601.toc> > > There is an introductory article that provides a brief overview of the > research: > > Paul R. Albert, Chawki Benkelfat, and Laurent Descarries (September 5, > 2012 ) > Introduction: The neurobiology of depression-revisiting the serotonin > hypothesis. I. > Cellular and molecular mechanisms Phil. Trans. R. Soc. B, 367, 1601 > 2378-2381; doi:10.1098/rstb.2012.0190 1471-2970 > > |Abstract > |The serotonin (5-HT) hypothesis of depression dates from the 1960s. It > |originally postulated that a deficit in brain serotonin, corrected by > antidepressant > |drugs, was the origin of the illness. Nowadays, it is generally accepted > that > |recurring mood disorders are brain diseases resulting from the > combination, > |to various degrees, of genetic and other biological as well as > environmental > |factors, evolving through the lifespan. All areas of neuroscience, from > genes > |to behaviour, molecules to mind, and experimental to clinical, are > actively > |engaged in attempts at elucidating the pathophysiology of depression and > |the mechanisms underlying the efficacy of antidepressant treatments. This > |first of two special issues of Philosophical Transactions B seeks to > provide > |an overview of current developments in the field, with an emphasis on > cellular > |and molecular mechanisms, and how their unravelling opens new perspectives > |for future research. > > There are 10 other articles in this issue that are relevant. > > -Mike Palij > New York University > [email protected] > > P.S. It would be a mistake to claim that it is a "lack" of serotonin that > is the > problem in depression because the drug tianeptine is a "Selective Serotonin > Reuptake ENHANCER" (SSRE), that is, it increases the amount of serotonin. > For one source, see the Wikipedia entry but a PubMed search may be > warranted: > http://en.wikipedia.org/wiki/**Tianeptine<http://en.wikipedia.org/wiki/Tianeptine> > I think it is fairer to say that depression is a dysreguation of the > normal levels of > various neurotransmitters and other neurochemicals. > > On Mon, 26 Nov 2012 07:45:12 -0800 , David Epstein wrote: > >> On Mon, 26 Nov 2012, Michael Britt went: >> >>> I recently received a couple questions about the effect of SSRIs on >>> depression and I'm not quite sure of the answer. Would anyone care >>> to edify us on these questions? >>> >>> Do people with depression produce enough serotonin, but it just >>> isn?t getting absorbed? In other words, it gets released and then >>> just hangs out in the synapse area? Or do they not produce enough >>> serotonin to begin with and what doesn?t get absorbed creates a >>> "deficiency"? >>> >>> As I understand it, SSRIs prevent serotonin from going back into the >>> originating neuron and MAOs destroy the serotonin left in the >>> synapse and that medication stops this destruction from >>> happening. Both of these are designed to keep the serotonin levels >>> high. Why not just increase the amount of serotonin in the body say >>> with 5-HTP supplement? Would more serotonin in the synapse allow >>> more to be absorbed? >>> >> >> My shortest, easiest answer--forgive me for doing it without giving >> cites--is that you can't think in global terms about there being "too >> much serotonin" or "too little serotonin." Serotonin is released >> along distinct pathways within the brain onto specific target regions, >> and it does different things in different regions. >> >> This is partly explained by (and partly just complicated by) the fact >> that there are at least 14 different subtypes of receptor for >> serotonin. The receptors aren't like the serotonin transporter that >> SSRIs block. They don't "absorb" serotonin; they're activated by it, >> the way a key on your computer keyboard is activated by your finger >> (without absorbing your finger!). >> >> What's more, the different types of receptor can change in number or >> sensitivity over the course of minutes, hours, days, weeks, or months. >> (The words to look up here and upregulation, downregulation, >> sensitization, and desensitization.) Those changes, which happen in >> slow and complicated ways in response to SSRIs and other >> antidepressants, are probably part of what makes the antidepressants >> work. >> >> OK? >> > > > --- > You are currently subscribed to tips as: [email protected]. > To unsubscribe click here: http://fsulist.frostburg.edu/**u?id=177920.** > a45340211ac7929163a02162444433**41&n=T&l=tips&o=21900<http://fsulist.frostburg.edu/u?id=177920.a45340211ac7929163a0216244443341&n=T&l=tips&o=21900> > or send a blank email to leave-21900-177920.** > a45340211ac7929163a02162444433**[email protected]<leave-21900-177920.a45340211ac7929163a0216244443...@fsulist.frostburg.edu> > -- Carol DeVolder, Ph.D. Professor of Psychology St. Ambrose University 518 West Locust Street Davenport, Iowa 52803 563-333-6482 --- You are currently subscribed to tips as: [email protected]. 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