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. 2015 Sep 8;6:931. doi: 10.3389/fmicb.2015.00931

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Copyright © 2015 Dahal, Chitti, Nair and Saxena.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Mechanism of Dopamine reuptake by DAT receptor (A) and blocking of the DAT receptor by cocaine and HIV Tat protein (B). (A). Dopamine, transmits brain signals by flowing from presynaptic neuron into the synaptic cleft and attaching to a receptor (DRD 1,5, and DRD 2,3,4) on postsynaptic neuron. In general, excess dopamine is recycled into the presynaptic neuron by a dopamine transporter (DAT) on the surface of the presynaptic neuron. The recycled dopamine is then degraded into homovanillic acid via monoamine oxidase (MOA). (B-a). In this case of cocaine drug abuse, the drug (cocaine) attaches to the DAT and blocks the normal recycling of dopamine, causing an increase of dopamine levels in the spaces between neurons that lead to inflammation. (B-b). The dopamine recycling is also inhibited by the Tat protein of HIV by bringing about conformational changes in DAT. The high concentration of dopamine in the synaptic cleft causes inflammation.