As with serotonin, the DA signal in the synaptic cleft is terminated primarily by reuptake into the presynaptic terminal. The dopamine transporter (DAT) comprises 12 putative transmembrane domains and is located somatodendritically as well as on DA nerve terminals (see Figure 1-4B). Like other monoamine transporters, the DAT functions as a Na+/K+ pump to clear DA from the synaptic cleft upon its release. However, data suggest that many drugs of abuse are capable of altering the function of these transporters. Thus, the amphetamines are thought to mediate their effects, in part, by reversing the direction of the transporter so that it releases DA. Cocaine is capable of blocking the reuptake of DAT, leading to an increase in DA in the synaptic cleft. Of interest, altered neuronal long-term potentiation in the VTA in response to chronic cocaine exposure has been recently linked to drug-associated memory and likely contributes to the powerful addictive potential of this drug of abuse (Q. S. Liu et al. 2005). DA in the medial frontal cortex is taken up predominantly by the NE transporter. Although the precise functional significance of this finding is not currently known, it goes against the dogma of transporters being able to selectively take up only their respective neurotransmitter. Furthermore, this provides a mechanism by which NE reuptake-inhibiting antidepressants may also increase synaptic levels of DA in the frontal cortex, effects that may be therapeutically very important.
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