DAT-CI mice contain the amino acid mutations L104V/F105C/A109V in exon 3 of the solute carrier family 6 (neurotransmitter transporter, dopamine), member 3 (Slc6a3) gene. Slc6a3 encodes the dopamine transporter (DAT) which pumps the neurotransmitter dopamine out of the synapse back into cytosol. Dopamine release in the ventral tegmental area (VTA) plays a major role in reward-motivated behavior. Defects in dopamine transport reduces the rate of transport from the synapse, thus increasing the levels of dopamine in the brain. DAT has been implicated in a number of dopamine-related disorders, including attention deficit hyperactivity disorder, bipolar disorder, clinical depression, and alcoholism. Cocaine is able to block this transport, by binding directly to the DAT, increasing reward-related dopamine activity. DAT-CI mice contain a triple mutation in the transmembrane domain 2 (TM2) of the dopamine transporter introducing a conformational change on the protein structure. These mice retain a functional DAT that is rendered insensitive to cocaine. DAT-CI DAT is 70-fold more insensitive to cocaine inhibition than WT mice.

DAT-CI mice contain a triple mutation in the dopamine transporter gene rendering them insensitive to cocaine.

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