Department of Psychiatry, Vanderbilt University School of Medicine, Nashville, TN, USA. > > Title..." /> Department of Psychiatry, Vanderbilt University School of Medicine, Nashville, TN, USA. > > Title..." />
Posted by Mitch on July 29, 2001, at 16:50:28
In reply to Re: Experience with trileptal? » Emme, posted by SalArmy4me on July 29, 2001, at 15:03:25
> It once was overwhelmingly helpful until it pooped-out (Tegretol XR).
>
> "Institution
> Department of Psychiatry, Vanderbilt University School of Medicine, Nashville, TN, USA.
>
> Title
> Valproate and carbamazepine increase prefrontal dopamine release by 5-HT1A receptor activation.
>
> Source
> European Journal of Pharmacology. 380(1):R1-3, 1999 Sep 3.
>
> Abstract
> The anticonvulsant mood stabilizers valproic acid (250, 500 but not 50 mg/kg) and carbamazepine (6, 12.5 but not 3 mg/kg) were found to increase extracellular dopamine levels in rat medial prefrontal cortex, but not nucleus accumbens. Increased prefrontal dopamine was completely abolished by the selective 5-HT1A receptor antagonist N-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-N-2-pyridinylcyclohexa necarboxamide (WAY100635, 0.05 mg/kg). Anticonvulsants and clozapine may share a common mood stabilizing mechanism since clozapine is reported to have mood stabilizing effects and increase prefrontal dopamine by 5-HT1A receptor activation."S4me,
This is a *little* off the subject, but this partially answers my question to you about the dopamine increase associated with 5-HT1a receptor agonism (in the case of buspirone). I became hypomanic on buspirone. Now I wonder about the potential antipsychotic efficacy of selective 5-HT *antagonists* which do not have any affinity for DA receptors (and possibly no EPS).
Mitch
poster:Mitch
thread:71844
URL: http://www.dr-bob.org/babble/20010725/msgs/72400.html