Posted by psychobot5000 on September 17, 2006, at 22:03:44
In reply to Re: lamictal and dopamine, posted by SLS on September 17, 2006, at 13:25:38
A very interesting hypothesis--hmm...I wonder whether the (anti) glutaminergic antidepressant/mood stabilizers in development right now would function in a similar manner...or...I don't know.
Thankyou very much for sharing your knowledge (and theory) on this!
> 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.
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...
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> 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.
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> 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.
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> :-\
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> - Scott
poster:psychobot5000
thread:686011
URL: http://www.dr-bob.org/babble/20060909/msgs/686964.html