You are of course right. It is a transporter protein which doesn't serve to cause serotonin mediated intracellular reactions.SERT isn't a receptor, and cannot be inhibited indirectly...
However, please explain what you mean by "cannot be inhibited indirectly". Afaik there are various ways to reduce SERT activity:
-Orthosteric/competitive inhibition (SSRIs)
-Allosteric/non-competitive inhibition (SSRIs)
-Dopaminergic pathways (d1 as well as d2 antagonists, but also tyrosine hydroxylase inhibitors can attenuate meth induced reduction of sert activity)
-Hyperthermia seems to be another mechanism responsible for meth induced sert inhibition
-There seems to be at least one additional yet unknown DA and hyperthermia independent mechanism by which Methamphetamine administration inhibits SERT
-I suppose the countless ways to downregulate SERT by inhibiting its expression don't belong here
So what exactly do you mean by your statement? I want to understand!
Absolutely.And as far as recreational drug effects go, there is a huge, huge difference between something increasing the release/firing of 5-HT downstream because of its actions on DA/NE; and being a SERT inhibitor or releasing agent.
Agree to disagree? Keep in mind the responses to 3FPM vary wildly, both dose-dependent and between subjects.IME there is nothing that stands out as serotonergic about the 3-FPM experience, although I agree it is less paranoia/anxiety inducing than many stims, I would attribute this more to its almost equal action at DA and NE as opposed to most stims having about double the EC50 for NE and also which areas of the brain is targets the most.