epoh, in terms of medications in this class (meaning what they are prescribed for, mind) all of the selective reuptake inhibitors are pretty much the same from a mechanistic standpoint. They may differ in terms of transporter/receptor selectivity and off-rate, downstream metabolites, etc. But fundamentally, the mechanism is the same.
Each works to increase concentrations of post-synaptic biogenic amine neurotransmitter(s) in the midbrain, via blockade of transport of that transmitter substance, (or, in the one mechanistic exception, to prevent its metabolism as in MAOI's); it's functionally operating via the same mechanism as the rest if it sits in a site that would be occupied by the neurotransmitter and locks up the active site.
It's worth noting, as well, that chronic (or just repeated) usage of anything in this class readily leads to habituation in a regulatory sense-- the system is remarkably well-protected from manipulation, having multiple feedback loops that result in up-regulation when you block transport. The upshot is that "rests" from medication may result in potentiated symptoms-- because of the system's determination to circumvent the pharmacology you've been applying.
This includes Adderall, Ritalin, SSRI's like Prozac, Xanax, as well as drugs like cocaine (which is horrifying in terms of being non-selective, btw). Withdrawal from ANY of those drugs is known to be a nightmare filled with anhedonia-- it makes addiction treatment incredibly refractory, because every additional use is not only "reinforcement" through the pleasure/reward pathway, but also because the withdrawal produces a LESS pleasurable baseline than in an untreated brain.
Are those drugs all "stimulants?" Well, clinicians judge "stimulant" on common responses to the drugs. Pharmacologists and neuroscientists don't classify things that way. Some of those drugs have known cardiac liability, of course-- but that is because they are pharmacologically "dirty" and act at cardiac receptors the way some biogenic amines do. Consider the structure activity relationships involved in a transporter/receptor that responds to dopamine or seratonin (5-HT), and then look at epinephrine (adrenaline). ALL of these drugs are, mechanistically speaking, analogs of one or more of those amines, in some way shape or form. Those which act elsewhere in the CNS as adrenomimetics are "stimulants." Caffeine is the one that most people are familiar with, but first generation AD(H)D drugs are generally this sort, as well. Those that act that way ONLY in the midbrain are considered "non-stimulant" drugs, or second gen therapeutics.
In terms of addiction potential-- there really is a genetic component to one's personal risk there. I have no idea how that overlays with AD(H)D, but drugs which act in this particular pathway in the brain? Yeah-- there is a range, of course, but generally speaking, some relatively small percentage of primates will NEVER become "addicted" and some also small percentage are addicts from the first use. In between fall the majority, which require from 3-25 uses to become permanently altered. It's an epigenetic effect, in other words, when you're talking about stimulant addiction potential. Methamphetamine is one of the most well-known drugs in this respect, though I'm more familiar with the literature re: cocaine, which was mostly produced two decades (or more) ago. Some people can use casually with impunity (but there are very few of them)-- and most people can NOT do that. That is a bit outside my area of expertise-- my recollection is that behavioral researchers were pretty busy trying to tease apart markers for which group an animal test subject belonged with, back in the early 90's (at least with amphetamine and cocaine, which were that era's "study drugs" of choice).
Last edited by HowlerKarma; 10/02/13 09:55 AM. Reason: it's a crying shame that I can't correctly type its.
