in DTBZOH binding in humans. Research suggests a decline in VMAT2 protein through prolonged cocaine use could play an important role in the development of cocaine-induced mood disorders. MDMA MDMA is known to affect serotonergic neurons, but has been shown to inhibit synaptosomal and vesicular uptake of serotonin and dopamine to roughly the same extent in vitro. In vivo studies indicate short-term MDMA exposure causes short-term reduction in VMAT2 activity, which is reversed after 24 hours. Current research Clinical research Genetic research models have shown that polymorphisms in SLC18A1 and SLC18A2, the genes that encode for VMAT1 and 2 proteins, respectively, may confer risk for some neuropsychiatric disorders; however, no specific diseases have been identified yet as directly resulting from a genetic mutation in an SLC18 gene, which codes for VMAT proteins. Much of the current research related to VMAT explores the genetic underpinnings of neuropsychiatric disorders as they may be affected by SLC18A'' family mutations. The dopaminergic neuron is known to play a central role in drug addiction and abuse and the potential role of the dopamine transporter has been well-explored as a target for amphetamine and cocaine. Current research looks toward VMAT2 as a target for such psychostimulants. A combination of imaging, neurochemical, biochemical, cell biological, genetic, and immunohistochemical evidence has been compiled to provide the most current comprehensive understanding of the role the VMAT2 plays in amphetamine and cocaine abuse and addiction through aminergic neurotransmission. As VMATs are membrane proteins, structural information is limited and researchers have yet to completely understand the structure of both isoforms. Further studies are needed in order to determine the structure and therefore complete function of these proteins. There is preliminary evidence that the gene for VMAT1 may be linked to susceptibility to schizophrenia, bipolar disorder, and various anxiety disorders. Further studies are needed in order to confirm these findings and to gain a better understanding of the role of VMATs in the central nervous system. Multiple single-nucleotide polymorphisms (SNPs) have been identified in the coding region of VMATs. The effects of some of these SNPs have been alteration of VMAT function, structure and regulation. Further investigation of these SNPs is required in order to distinguish whether they may be attributable to certain diseases with suspected SNP-mutation origins. α-synuclein, a cytosolic protein found mainly in pre-synaptic nerve terminals, has been found to have regulatory interactions with the trafficking of VMATs; mutations involving