Editing Vesicular monoamine transporter (section)

===Cocaine===
Unlike methamphetamine, cocaine interacts with VMAT2 by mobilizing VMAT2-expressing vesicles, causing a shift in VMAT2 proteins from a plasmalemmal (synaptosomal) membrane fraction to a vesicle-enriched fraction that is not associated with the synaptosomal membrane and not retained in synaptosomal preparations.<ref name="Wimalasena, K. 2011"/><ref name="Chaudhry FA 2007"/><ref name="Fleckenstein AE 2007"/> Methylphenidate is believed to interact with VMAT2 in a similar fashion.<ref name="Fleckenstein AE 2007"/>

In addition to mobilizing VMAT2-expressing vesicles, cocaine has been shown to increase the V<sub>max</sub> of VMAT2 for dopamine and increase the number of DTBZ binding sites.<ref name="Chaudhry FA 2007"/> It has also mobilized a [[synapsin]]-dependent reserve pool of dopamine-containing synaptic vesicles, which interacts with the vesicular trafficking cycle to increase dopamine release.<ref name="Chaudhry FA 2007"/>

Short-term exposure to [[cocaine]] increases VMAT2 density in the [[prefrontal cortex]] and striatum of mammalian brains. This is theorized to be a defensive mechanism against the depletive effects cocaine has on cytosolic dopamine through increasing monoamine storage capacity.<ref name="Wimalasena, K. 2010"/> Chronic cocaine use has been implicated with a reduction in VMAT2 immunoreactivity as well as a decrease 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.<ref name="Wimalasena, K. 2010"/>