Posted by Shawn. T. on July 12, 2002, at 21:59:24
In reply to Re: Some antidepressant theory, posted by cybercafe on July 12, 2002, at 1:13:13
Awesome, thanks for your help. I haven't had time to do any reading on dopamine; what you told me is really fascinating. I can really put that information to good use! You really clued me in on 5-HT4 action as well. My interest in moving beyond 5-HT2 receptors (yes, that is my primary interest because of Remeron) has brought me away from serotonin and dopamine receptor research. I've been really into hormones recently if you haven't notice. There is definitely much more to depression than serotonin, despite what SSRI producing companies would like you to believe. You should see how many IE windows I have open at once all the time (I try to keep it under 18).
I am really blown away by evidence linking intelligence to depressive symptoms and lack of it to euphoria. I have an IQ of 135 or higher (not bragging, just illustrating a point) and am
not the happiest guy in the world when not on drugs by any means. You may be intrigued by the fact that Remeron+Wellbutrin has entirely curtailed my drug abuse.As for 5-HT3, I believe there are definitely lots of pro's and con's to blocking this receptor. This is a complicated receptor, and I don't know whether or not I'm glad mine is being antagonised or not.
5-HT5 receptors interact negatively with adenylyl cyclase. So their activation decreases adenylyl cyclase activity. That would seem to signal a decrease in cortisol. Another anti-depressant mechanism of serotonergic agents, perhaps? Also, a possible explanation of seasonal affective disorder?
http://www4.infotrieve.com/search/databases/detailsNew.asp?artID=25950478Based on five minutes of reading, antagonists of 5-HT6 receptors appear to increase glutamate (excititory neurotransmitter) levels. That means cognitive enhancement without a doubt. I'll update you on more about this later.
You might be interested in my theory of SSRI related male sexual dysfunction. 5-HT1a activation in combination with 5-HT2a and 5-HT2c leads to increased prolactin excretion. Increased levels of prolactin lead to hypogonadism, with decreased sex drive, decreased sperm production and possible impotence. It also makes your breasts larger. I can't wait for M,100,907 (the 5-HT2 selective antagonist) to be released.
I believe 5-HT1f may be linked to migraine headaches. 5-HT1f controls contraction in vascular, urinary, gastrointestinal, and uterine functions. Migraines cause vascular dilation (not sure if that's the word I want) I believe.
Check this out on aggression too:
http://www.biopsychiatry.com/aggression.htmAlso 5-HT1a agonists seem to cause up-regulation by the way. This makes me think that taking an SSRI after consuming MDMA really is a good idea.
The increase in serotonin caused by an SSRI would prevent serotonin receptor up regulation in response to a massive serotonin decrease after taking MDMA.
http://mdma.net/mdmaeff.htm
Makes me wish that I hadn't done ecstacy (I've done it all, and I'm now going about undoing what damage I may have done hahaha).Something tells me this might spark your interest.
http://www.tocris.com/cat/5ht567.html
poster:Shawn. T.
thread:111957
URL: http://www.dr-bob.org/babble/20020709/msgs/112168.html