Posted by bornunderabadsign on February 12, 2001, at 4:33:41
I considered this over my Cap'n Crunch this morning:
Given the two states of dopamine transmission: Basal and Pulsatile, how does amisulpride effect such transmission. When should it work and when should it not work.
I tried amisulpride 10mg/day for a month, and noticed no subjective mitigation of symptoms.I have just started wellbutrin sr 150mg/day. My idea is this:
Pulsatile, or hyperpolarization-modulated DA exocytosis is believed to be regulated by presynaptic Auto-Receptors, which Amisulpride is believed to act upon.
My hypothesis is this: Basal, or "backround" levels of DA are regulated by the amount of DA transport in the synapse. Therefore, such an inverse relationship can be stated:
1
_______________________ = level of DA transportEfficacy of Amisulpride
Moreover, it is possible that Wellbutrin modulates basal level of DA, and, therefore the workings of DA transport.
Indeed, Wellbutrin is anything but immutable, sometimes making things worse, and sometimes better. Wellbutrin blocks Dopamine (DA) *reuptake*, while, at the same time *decreasing* release.
Obviously, I have conducted no formal trial of such a hypothesis, however, these phenomenon may support it:
1.) Greater success of Amisulpride in Wellbutrin-resistant patients.
2.) Less success of Amisulpride in those who recently built a tolerance to psycho-stimulants.
3.) Less signficant success, or failure, of amisulpride in Wellbutrin-successful patients.
Not sure, but any comments would be welcome. I should know in a few weeks if the wellbutrin works for me where Adderall has gradually failed.
Elvis has left the building,
-James
poster:bornunderabadsign
thread:53790
URL: http://www.dr-bob.org/babble/20010212/msgs/53790.html