Nueroresearchers such as Eric Braverman understand the huge importance of GABA.
Being the main inhibitory neurotransmitter, it doesn't take a PH.d researcher to see that its rather important, though, so is NMDA, so are the big three sympathetic, dopamine, norepinepherine and serotonin, so is Ach. Raise or drop the levels of ANY of them drastically and generally, some failure mode resulting in death occurs. Play with a little too much, and something unejoyable happens (be it anxiety, seizures, dyskenesias, hyperthermia, psychotic episodes or other eratta problems resulting from CNS regulation being whacked out)
But that wasn't my first point, my first point is exogenous agonist does not equal increasing organic agonist...say for example, exogenous 5HT ligand LSD is not the same as force release of 5HT by MDMA, nor is it the same as serotonin toxidrome. (I think if it had the disseminated vascular coagulation, it wouldn't be as popular as it is.)
exogenous DA antagonist pimozide is a little more severe then lack of DA after an amphetamine binge. (I don't get permanent motor dysfunction from a comedown)
There is a significant difference between the varied exogenous ligands, and the organic one (or depletion of organic one vs blockade by antagonist) the effect is NOT the same, it can be markedly different and very different depending on which synthetic it is. thiopental is just a tad different from gabapentin, wouldn't you say?
and parkinson's re GABA: yeah, it might have some role, but I think the case is pretty solid on parkinson's being primarily DA related.
This wasn't a rant about big pharma or the mental health system, it was about not abstracting two different things into being identical.