Posted by SLS on June 25, 2005, at 21:30:33
In reply to But wait ? How does this make sence?, posted by linkadge on June 25, 2005, at 19:11:24
> I've never really had a decent explaination of this concept. If depressed people really had an altered reputake mechanism for serotonin, then why don't "normal" people have sexual side effects, insomnia, and dystonia.
Thinking out loud...
The dynamics of the system include many feedback loops that help keep it running at a nominal velocity. Perhaps people with the each version of the 5-HT transporter display a different complementary rate of second messenger events and the expression of varying numbers of membrane receptors. For example, there is a *higher* number of 5-HT2a post-synaptic receptors found post-mortem in suicide victims. Yet, 5-HT1a autoreceptors are upregulated as well. It is counterintuitive to think that a reduced rate of reuptake would produce such a state, except that the upregulated autoreceptors work to reduce the rate of synthesis and release of serotonin. This would help to balance a sluggish reuptake system. It seems to me, however, that such a system would not tolerate perturbations very well. There isn't much room left for homeostatic mechanisms to compensate for stress and overactivity. On the other hand, a greater number of transporters allows for greater variation in the sensitivities of receptors to maintain homeostasis during stressful times because they are not upregulated to begin with.
- Scott
poster:SLS
thread:518841
URL: http://www.dr-bob.org/babble/20050622/msgs/518934.html