Talk:Dopamine transporter

Difficult for non-specialist to understand
This page is written in a way that is virtually impossible for a non-specialist to understand. For example, one can not tell if the transporter is a physical structure that moves the dopamine or a chemical that binds to it, or both. 66.245.159.152 23:21, 6 March 2007 (UTC)Andrew Hoerner

I'm currently working on a relatively large scale revamp/expansion of this page. It will include a lot more detail on the nature of the protein as well as the structure of the gene and some associations with diseases/disorders.Dylanalegria 19:35, 5 June 2007 (UTC)

The localisation section needs more references. The statement that DAT is not present at active synapses is based on one report! —Preceding unsigned comment added by 138.38.26.187 (talk) 11:07, 17 January 2008 (UTC)


 * Andrew, as it happens, all "physical structures" are made up of chemicals. The answer to your question is "both".  WhatamIdoing (talk) 18:18, 21 June 2008 (UTC)

Removal of incorrect statement
This sentence "This does not apply to the prefrontal cortex where dopamine is reuptaken by the norepinephrine transporter[1], which is less effective for this purpose. Hence, dopamine in the prefrontal cortex spreads and persists longer than in other parts of the brain where DAT terminates the dopamine signal." is outrageously incorrect. First of all, this study was not done in wildtype mice. Only DAT and NET knockout mice were used. Hence this finding cannot be generalized to all mouse lines. Study from wildtype is very essential to draw any conclusive inference on this. On the contrary, there is evidence to suggest that DAT plays a huge role in frontal cortex, especially in humans, and pharmacological evidence using SPECT and fMRI suggest that congnitive function in frontal cortex is chiefly dopamine responsive whereby its action is chiefly determined by DAT. Therefore, I have removed this sentence. —Preceding unsigned comment added by 212.149.207.239 (talk) 13:40, 6 June 2009 (UTC)

Cocaine as an Na/sodium Channel blocker of the cellular wall and DAT's mechanism of action
Could the action potential of cocaine be what makes it so much more highly potent of a DRI than other DRI's of non-generalized-sodium channel effecting classes, when administered IV? (So that the sodium channel blocking effects are not squandered on epidural membrane walls and other protective, effect reducing barriers against external substances)? 71.237.187.95 (talk) 19:39, 6 July 2010 (UTC)

Localization: Synaptic Active Zones
"Surprisingly, DAT was not identified within any synaptic active zones. These results suggest that striatal dopamine reuptake may occur outside of synaptic specializations once dopamine diffuses from the synaptic cleft." I believe active zones are small areas with high density of proteins, not the entire presynaptic membrane. This would mean DAT could still be located on in the synapse, and if so dopamine would not have to leave the synapse for reuptake. I'm also not sure whether this localization is in fact surprising. Also, we probably need a citation for DAT not being located in active zones. TalkPageWarrior (talk) 14:10, 25 June 2016 (UTC)