Dataset for: Constitutive plasma membrane monoamine transporter (PMAT, Slc29a4) deficiency subtly affects anxiety-like and coping behaviors

Originally, uptake-mediated termination of monoamine (e.g., serotonin, dopamine) signaling was believed to only occur via high-affinity, low-capacity, transporters (“uptake1”) such as the serotonin or dopamine transporters, respectively. Now the important contribution of a second low-affinity, high-capacity, class of biogenic amine transporters has been recognized, particularly in circumstances when uptake1 transporter function is reduced (e.g., antidepressant treatment). Pharmacologic or genetic reductions in uptake1 function can change locomotor, anxiety-like, or stress coping behaviors. Comparable behavioral investigations into reduced low-affinity, high-capacity transporter function are lacking, in part, due to a current dearth of drugs that selectively target particular low-affinity, high-capacity transporters, such as the plasma membrane monoamine transporter. Therefore, the most direct approach involves constitutive genetic knockout of these transporters. Other groups have reported that knockout of the low-affinity, high-capacity organic cation transporters 2 or 3 alters anxiety-like and stress coping behaviors, but none have assessed behaviors in plasma membrane monoamine transporter knockout mice. Here, we evaluated adult male and female plasma membrane monoamine transporter wildtype, heterozygous, and knockout mice in locomotor, anxiety-like, and stress coping behavioral tests. A mild enhancement of anxiety-related behavior was noted in heterozygous mice. Active coping behavior was modestly and selectively increased in female knockout mice. These subtle behavioral changes support a supplemental role of plasma membrane monoamine transporter in serotonin and dopamine uptake, and suggest sex differences in transporter function should be examined more closely in future investigations.