Editing Vesicular monoamine transporter (section)

==Inhibition==
The effects of VMAT inhibition have been studied in-depth in animal models. Mutant [[homozygous]] VMAT(-/-) mice move little, feed poorly, and die within a few days of birth.

More specifically, inhibition of VMAT2 may cause an increase in cytosolic catecholamine levels, which can result in an increase in efflux of catecholamines through the [[cell membrane]], depleting catecholamine concentrations and causing increased [[oxidative stress]] and oxidative damage to the neuron.

[[Heterozygous]] VMAT [[Mutant|mutants]] display hypersensitivity to [[amphetamine]], cocaine, and [[MPTP]] (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), the latter being a substance causally linked to [[Parkinson's disease]] (PD) in rodents.<ref name="Brunk, I. 2006"/> This suggests a protective role of VMATs against oxidative stress through removal of such substances from the cytosol.<ref name="Brunk, I. 2006"/>

VMAT inhibitors include:
*Reserpine (RES), [[bietaserpine]], and [[ketanserin]] (KET) (potent inhibitors of VMAT2 mediated serotonin transport)
*[[Tetrabenazine]] (TBZ) (specific to VMAT2)
*[[Phenylethylamine]]
*[[Amphetamine]]
*[[MDMA]]
*''N''-Methyl-4-phenylpyridinium (MPP<sup>+</sup>) (very potent inhibitors of VMAT2 mediated serotonin transport)
*[[Fenfluramine]] (specific to VMAT1 )
*[[5'-Guanylyl imidodiphosphate|Non-hydrolysable GTP-analogue guanylyllimidodiphosphate]] GMP-P(NH)P (VMAT2 only)