ADD and Ritalin

Jason Kennerly jkenner at cello.gina.calstate.edu
Fri Sep 1 20:04:50 EST 1995


fboix at pons.uio.no (Fernando Boix) writes:
> >I don't know if anyone actually knows exactly.  One theory I've heard is that 
> >GABAergic transmission is lower than it should be in certain areas.  Ritalin, 
> >according to this theory, is supposed to stimulate GABA transmission.  This 
> >results in a net inhibitory effect, and is supposed to be why Ritalin reduces 
> >the hyperactivity and increases ability to concentrate.  I don't know if the 
> >theory has much evidence for or against it (I've seen a few studies advancing 
> >the theory, but I didn't really look at them in depth), nor do I know of other 
> >theories that are out there.  It's not really my specialty, but maybe this can 
> >give you a jumping off point for further research.  Good luck.

> Methylphenidate, the active compound of Ritalin, is a potent dopamine
> uptake blocker, like cocaine, increasing the concentration of this
> neurotransmitter in the synaptic cleft and increasing, therefoere, the
> dopaminergic neurotransmission. Amphetamine, which is also used in
> ADD-ADHD, also increases dopamine neurotransmission but in another way
> (not very good known but it seems it increase dopamine release by
> reversing the uptake mechanisms). 

Some good points here. Yes, Ritalin is indeed a potent dopamine reuptake 
blocker, also effective norepinephrine [about 1/5th as much as it effects 
the dopamine transporter according to a recent article on bromine analogs 
of methylphenidate I just read].

I've also heard that amphetamine reverses the dopamine transporter, 
presumably by "clogging it" and allowing higher concentrations of 
dopamine to diffuse out of the cell. The designer-drug MDMA, related 
vaguely to amphetamine, has been shown to increase release of serotonin 
INDEPENDANT of neuronal firing, suggesting it also works this way.

Prozac, and other SSRI's have been reported to decrease the effects of 
MDMA if administered several hours prior to taking the MDMA. Presumably 
it competively occupies the transporter, blocking reuptake of serotonin 
while preventing MDMA from getting in and inducing release...

This might nicely explain why although Ritalin and Dexedrine work 
slightly different they are rarely used in conjunction - it could be 
counterproductive (!), if the observation of inducer to reuptake blocker 
relationships were to extend to the dopamine transporter as well... does 
it? I really dont know...

Also worthy of note... I saw an abstract that suggested that dopamine in 
the presence of d2-inhibitors does indeed potentiate GABAergic systems. 
The general suggestion was that some other dopamine receptor was 
intimately involved with GABA systems, but that the stimulatory effects 
of activating the d2 receptor made it hard to observe... comments anyone?


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