Posted by psychobot5000 on February 22, 2007, at 22:49:58
In reply to Re: Lamictal and nicotinic acetylcholine receptors, posted by circusboy on February 22, 2007, at 22:30:23
>>...using the adult muscle nicotinic acetylcholine receptor as a model system. At the single-channel level, lamotrigine caused a dose-dependent (a) diminution in mean open time, (b) increase in mean burst duration and (c) increase in the area of a new closed-time component. A simple linear channel blocking mechanism accounts for these results. Thus, lamotrigine exerts a blocking action on the muscle nicotinic acetylcholine receptor.
>
> PMID: 17259859I think that it's saying that lamotrigine causes a change in firing rates in these nicotinic pathways, and that these are consistent with 'a simple linear channel blocking mechanism,' by which I think they mean the sodium channel blocking. I believe anti-epileptics that effect sodium channels and glutamate change the firing rate and amplitude of nerve signals all over the body--sodium channels are pervasive. So if I read this right (I may not be), I think it's not being seen particularly as anticholinergic or antinicotinic--that's just the area they're checking in this study, and it's 'consistent' with lamotrigine's (and other AEDs') effect on sodium or maybe calcium channels.
Someone else may have a better understanding of this.
poster:psychobot5000
thread:734880
URL: http://www.dr-bob.org/babble/20070219/msgs/735246.html