Posted by Chairman_MAO on February 12, 2004, at 19:38:17
In reply to ChairmanMAO-lamictal AD props, posted by jaby on February 12, 2004, at 10:08:02
Ugh, I had a post prepared of what I could make sense of on medline about this, hit the wrong button in my browser, and then my post disappeared (dr-bob.org doesn't seem to be totally compatible with Opera).
Lamictal's AD action is really beyond the scope of my knowledge, but I'll summarize, since I'm having some nausea from the Wellbutrin I just started and want to lie down.
The gist of what I was saying is that lamotrigine's antiepileptic actions are not fully elucidated, let alone its mechanism in mood disorders. However, as I understand it, it both blocks some GABAnergic activity and increases GABA concentrations [with chronic administration]. It's a sodium channel blocker (and blocks certain calcium channels, I have no idea what the certain subtypes even mean at all, so I'm the wrong person to ask), but AFAIK prevents kinds of seizures other Na+ channel blockers don't; however, I don't think it's Na+ blocking action is relevant to the antidepressant effect; that is probably due to [indirect] inhibition glutamate [and aspartate?] release. If you search medline, you'll see some studies even contradicting each other. Lamotrigine probably has a mechanism involving modification of intracellular signalling or something completely different from just affecting neurotransmitters (and so is the end result of antidepressant treatment, FWIW). I think lamotrigine does downregulate beta-adrenoreceptors, just like conventional antidepresants.
I wish I could tell you more, but I'd be lying if I didn't admit that lamotrigine's actions go way over my head.
poster:Chairman_MAO
thread:312412
URL: http://www.dr-bob.org/babble/20040210/msgs/312587.html