Because I don't believe that I had ever thought about the question that Michael Britt posed, I really appreciated the question itself and most certainly the thoughtful responses by David and Mike. I probably can say the same thing just about every week but being that Thanksgiving has just passed ... well ... yeah ... thank you, TIPS.
Miguel ----- Original Message ----- From: "Mike Palij" <[email protected]> To: "Teaching in the Psychological Sciences (TIPS)" <[email protected]> Cc: "Michael Palij" <[email protected]> Sent: Monday, November 26, 2012 11:34:06 AM Subject: Re: [tips] Questions about Serotonin and Depression 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 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 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=466839.0421d1005414eed82340aa280e7ce629&n=T&l=tips&o=21900 or send a blank email to leave-21900-466839.0421d1005414eed82340aa280e7ce...@fsulist.frostburg.edu --- You are currently subscribed to tips as: [email protected]. 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