Posted by Scott L. Schofield on January 31, 2000, at 11:35:50
In reply to Scott, Ant, posted by Adam on January 30, 2000, at 15:48:28
> As for my curiosity about my own genetic makeup, I've thought about the experiment since then, and there are a lot of potential problems that could make it not really worth doing. Also, if my 5-HT2A receptor were defective, then how can I explain my reaction to Serzone mechanistically, or the fact that I did not have such an adverse reaction to Remeron, which is also a 5-HT2 antagonist (though it does a number of other things too, just like Serzone).
It seems that the serotonin synapse is quite complex. There are different types of receptors all over the place. I really haven't focused on the details of these sites, but there are a few things that come to mind. I noticed that you specified the 5-HT2a as the receptor transcribed from the "defective" gene. Are there more than one type of 5-HT2 receptor? If there are, perhaps differences in the drugs' binding selectivities could account for the apparent inconsistency of observations. Pharmacokinetics may also be a determinant in your differential reactions to Serzone versus Remeron.
Would these two drugs produce a different ratio of receptor activity due to their behaviors at other serotonin sites, for instance, 5-HT3? Perhaps the ability of Remeron to antagonize presynaptic alpha-1 noradrenergic receptors and the resultant increase in NE activity provides an offset to, or shunt of, the suspect serotonergic pathways. Histamine?
All of these questions would be immensely fascinating, if the answers weren't so critical to our lives.
Does anyone care to summarize the features of the serotonin synapse?
- Scott
poster:Scott L. Schofield
thread:19909
URL: http://www.dr-bob.org/babble/20000128/msgs/20186.html