Posted by desolationrower on September 13, 2009, at 1:52:59
In reply to Re: Dopamine Pathways Implicated in Adult Add Adhd, posted by linkadge on September 12, 2009, at 7:00:11
> But, how would stimulants ameleorate this?
>
> Stimulants typically lower the levels of DAT and the expression of post synaptic dopamine recpetors.
>
> It seems to me that an AD would be better at fixing these abnormalities. SSRI's typically increase the expression of DAT and increase the sensitivity / responsiveness of mesolimbic dopamine recpetors.
>
> Linkadgethe reduced da sensitivity after treatment is 'tolerance' - it means your first few weeks you can use a lower dose. like going on a diet slows your metabolism, but still make you thin. the body compensates, but the drug can still keep you at a new equilibrium.
and i kind of remember the hyperactive->hypoactive course of disease has something to do with DA changing from over to underactive, so it probably has to do with maturation as well as just equilibrium-maintaining regulaiton, like overexpression early in life caused overreaction in the developing brain.
anyway, dnris ritalin/cocaine increase DAT expression. AMP decreases DATs. and selegiline increases expression of 'nonfunctional' DATs.(lolwtf)
i wonder if NRI effect which is often said to 'take two weeks' is mostly the reverse tolerance aka dopaminergic sensitisation that is also seen on stims. i don't otherwise can explain why blocking NAT wouldn't increase catelcholaminergic transmission w/in hours. unless cortical effects only become notcible after days even for stims, but this is masked.
certainly feels right for me, APs felt like my adhdi problem, just concentrated into pill form.
-d/r
poster:desolationrower
thread:916581
URL: http://www.dr-bob.org/babble/20090912/msgs/916809.html