The general assumption is that they will have similar effects, but until then it's only theory.
Prozac is the popularly mentioned SSRI in MDMA neurotox research because it has been the best studied. Several other SSRIs such as citalopram have also been found effective, and there is every reason to believe the effect is a quality of the entire drug class, not just Prozac.
I am uncomfortable with the idea taking of SSRIs to try to protect against MDMA neurotoxicity because at least if taken after the fact they are unlikely to offer more than partial protection if conditions for damage have otherwise been met. In rat studies, damage appears to be occuring in as little as an hour from giving them MDMA; the oft-quoted 'six hours later' figure is the latest time Prozac still had any effect; extensive damage had already occurred at that point.
Given the critical role of overheating and oxidation in MDMA neurotoxicity, the best advice I can give is to take antioxidants before use, avoid hot environments if you're going to be active (dancing) and never mix with other stimulants (or additional doses of MDMA for that matter.)
There is an enzyme called MonoAmine Oxidase present in the area of the axon in which seratonin is reabsorbed...it's job is to break 5ht (seratonin) back down. Well, it is incapable of effectively breaking down dopamine, causing the dopamine to behave as a free radical, damaging the axon
Producing oxidizers is actually normal for many enzymes that break down chemicals, including I presume MAO. (Converting sugar into energy is a major source of oxidizing chemicals in cells.)
The idea of dopamine as the source of toxicity has been clarified; rather than being the immediate source of oxidization, dopamine's role seems to be limitted to promoting the overheating needed for neurotoxicity. (Animals depleted of dopamine can suffer the same degree of damage as normal ones.
Reference.)
My personal theory is that decomposition of MDMA itself by MAO is occurring, with that process being the source of oxidizing chemicals. (MAO is critical to neurotoxicity, and rat experiments have shown that
something in the brain agressively breaks down MDMA.) It's only a theory at this point, but I'd put about 85% odds on it.
and causing it to curl away from it's associated dendrite. This increases the size of the synapse, requiring your body to produce more of any neurotransmitter in order to pass the same electric impulses from the axon to the dendrite.
In MDMA neurotoxicity, the axons appear to lyse (break open) and be completely destroyed. An 'injury' to the axon that still left it structurally intact should be recovereable.
Synapses are often drawn as open empty spaces, with the neurons just sort of 'floating' nearby each other. Fortunately for us, neurons actually anchor to each other across the synapse, making it very hard for them to come apart.