Posted by SLS on September 17, 2006, at 13:25:38
In reply to Re: lamictal and dopamine, posted by psychobot5000 on September 17, 2006, at 12:41:48
Right now, the main actions that Lamictal is known for is to block sodium channels, some calcium channels, and to inhibit the release of glutamate.
There must be some reason for the presumed transient release of dopamine - probably in the nucleus accumens - that is probably secondary to one of these three properties or perhaps primary to one that has not been discovered yet. It might be due to an abrupt change in the degree of inhibition of release of glutamate in the thalamus, which would lead to increased DA release in the NucAcc (by decreasing kainate glutamatergic receptor activity there).
So...
You raise Lamictal, it goes to the thalamus, it enters glutamate neurons, it inhibits the release of glutamate into the synaptic cleft, the glutamate neuron across the cleft does not fire. That neuron, which travels on to the nucleus accumbens, is inhibitory upon DA neurons (acting in concert with GABA neurons), and normally prevents DA neurons from releasing DA. However, without this thalamic glutamate neuron firing, we have no inhibition, so this nucleus accumbens DA neuron is free to release its DA.
Now you feel good - for awhile. The problem is, it doesn't last. Why doesn't it last? I don't know. Is it because you run out of DA because the enzymes can't keep up with demand? Hmm. Unlikely. Is it because... I'm not going to start this right now.
:-\
- Scott
poster:SLS
thread:686011
URL: http://www.dr-bob.org/babble/20060909/msgs/686817.html