he cell. To begin, studies have proven that dopamine itself could be extremely toxic to the cells. However, the real problem occurs when dopamine encounters the MAO. The MAO oxidizes the dopamine and forms hydrogen peroxide. This substance is deadly to the nerves so that when it is released that part of the axon will die.The proof comes from many former studies in the field that led them to postulate this theory of deterioration. In 1988, studies done by a team of scientists led by Stone found that treating mice with a-methyl-p-tyrosine prevents the normally observed axon terminal degeneration. This substance is proven to prevent the release of dopamine, so they hypothesized that with the lack of dopamine, the MDMA would not have its normal effects of neurotoxicity. Other studies suggest the same thing. One such, performed by Schmidt et al., was conducted so that they destroyed the dopamine terminals in the rats’ brains, receiving the same effects and also attributing the effect to the lack of dopamine. Also in 1990, two researchers, Nash and Nichols, proved that if you add the substance L-DOPA, the damage sustained is much greater, presumably because L-DOPA is a stimulant to the dopamine receptors, which works a great deal like MDMA. However, since dopamine is considered a robust system, the brain’s reserves cannot be used up as quickly as those of serotonin (Sferios).Dopamine’s effect is also extended as a side effect of MDMA itself. MDMA’s serotonin release also affects a serotonin receptor, called receptor 2A, which by itself is a precursor to the release of dopamine (Sferios).It has been proven that axon terminals can regenerate themselves, however poorly, and in bad condition. Some studies suggest that even the appearance of axons affected by MDMA is swollen and heavily distorted (Ricaurte). The serotonin nerve cells, when deteriorated in this way, are prone to reform further down the axon (Cl...
