Posted by linkadge on July 25, 2006, at 17:06:15
In reply to Re: what is my problem » linkadge, posted by SLS on July 24, 2006, at 23:20:03
The thing that interested me about 5-ht1b autoreceptor antagonists, is that they are able to increase serotonin in selective areas of the brain, like the hippocampus. The reason I think that serotonin uptake is not involved is because in order to get a downregulation of serotonin autoreceptors, you need to take enough to completely wipe out sexual behavior.
You take an SSRI, you will get some increase in hippocampal serotonin, but at the expense of serotonin in the amygdala, and serotonin in the part of the brain regulating sexual behaviors.
The 5-ht moduline, is an endogenious 5-ht1b autoreceptor antagoinsts. Suppose, that the acitivity of this agent was out of whack for some reason. This would result in low levels of serotonin in certain areas of the brain.
Take a look at this agent.http://biopsychiatry.com/sb-236057.htm
Its a 5-ht1b autoreceptor invere agonist. It seems to selectivly increase seronin in the dentate gyrus in a similar manner to paroxetine.
The 5-ht moduline, and lithium essentially do the same thing. They block the 5-ht1b autoreceptors and increase serotonin release in the hippocampus.
That is very significant. This is where we want the serotonin to promote neurogenesis.
Linkadge
poster:linkadge
thread:669157
URL: http://www.dr-bob.org/babble/20060724/msgs/670424.html