Do antidepressants(such as Prozac) function similar as cocaine and ecstasy?

Question

don't antidepressants block the reabsorptions of serotonin, norepinephrine and dopamine, thus boost depressed people's mood? but then don't they function the same as what drugs(such as cocaine and ecstasy) do to our body? does prolonged use of antidepressants destroy serotonin-producing neurons like what ecstasy does? does repeated use of antidepressants deplete our productions of serotonin, norepinephrine and dopamine?

Answer 1

from what i know SSRI's dont effect norephinephrine unless its something like effexor. but thats called an SNRI.

i also dont think it has a significant effect on dopamine. however the function of an ssri block the reabsorption of seritonin in the same way cocaine blocks dopamine. ecstasy also just releases a massive amount of seritonin into the synapses. both drugs though are shoter duration than with antidepressants.

the sereitonin depleteing properties of ecstasy have been found to be mostly done by poor studies. the depletion appears to be temoporary and can actualy be reversed just by using a 5HT-p supplement to help restor seritonin. there is no significant danger to ecstasy or its neurons other than overheating or ending up with something that the pill has been cut with.

there has been reported long term side effects of people who have used SSRis for long periods of time. and some still have those effects long after use has stopped.

SSRIs may cause other long term damage but not very many studies have been done. after all, its a major money market for them. they arent gonna pull them any time soon.

Answer 2

Antidepressants reduce resorption. Remember, when you're working in biology, you can't block 100% of an enzyme, or block 100% of the receptors. There are antidepressants that work on dopamine and norepinephrine(SNRIs, wellbutrin, MAOI, TCAs) but the conventional SSRI ADs do not.

For cocaine it's a matter of strength, cocaine at even small doses inhibits the dopamine reuptake transporter immensely. As I said, you can't get to 100%, but you can get far, far too much. I don't know that cocaine is specifically associated with a brain damaging mechanism itself. Most of the damage seems to come from cardiovascular problems - strokes and heart attacks and aneurisms. That sort of thing. A dopamine reuptake inhibiting drug like Wellbutrin is significantly less potent, to the point where you'd have to take bottles of it to get the same effect. Another example would be methamphetamine. We use 1-2mg in the form of Desoxyn for certain conditions, but when abused people take hundreds to thousands of times that does to get high.

Ecstacy is a messier case, ecstasy causes release of vesicles containing serotonin (and other neurotransmitters), but it also disables a large number of the reuptake transmitters by causing them to pump -backwards- dumping free serotonin from inside the nerve to outside it. This causes a massive, massive build up in serotonin, as the mechanisms for clearing it are largely disabled. To date, no antidepressant has anything resembling this mechanism. It's also unclear wether the serotonin nerves themselves are dying, or the glutamate neurons they are adjusting are dying (difficult to measure, conflicting info) but the result is the same, the system stops working correctly because nerves are dead. There's no indication that any antidepressant causes nerve death (TCA's are toxic to heart muscle if you get enough of them and they 'spill over' - why we don't use them). We do know that SSRIs cause increased nerve growth in the hippocampus.

Actually messing with the production of antidepressants is -extremely- difficult to do. The body does not tolerate interference with it, which is why you can't induce serotonin syndrome with 5HTP, and why L-Dopa stops working after repeated doses. There are very few drugs that even indirectly affect production (THC may be one, Anandamide the natural neurotransmitter is implicated in brain metabolism). The best we can do is inhibit breakdown - via MAOI which by and large the body does not seem to develop tolerance to.

While on paper the phrase "inhibits reuptake" is the same for both, the molecular stories are actually quite different.