【摘 要】
：
Cocaine, an addictive drug of abuse, increases the extracellular dopamine (DA) concentration in the basal ganglia, which is previously assumed to occur mainly through the inhibition of the reuptake ac
【机 构】
：
State Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Molecular Medicine, Pek
【出 处】
：
The 9th Asian Biophysics Association Symposium (ABA2015)(第九届
论文部分内容阅读
Cocaine, an addictive drug of abuse, increases the extracellular dopamine (DA) concentration in the basal ganglia, which is previously assumed to occur mainly through the inhibition of the reuptake activity of DA transporter (DAT).Under physiological in vivo conditions, however, it remains unclear whether cocaine affects DA release as well.Here, we report two kinetically distinct DA releasable vesicle pools, a fast-releasable pool (FRP) and a prolonged-releasable pool (PRP) in mouse striatum following physiological frequency stimulation of the medial forebrain bundle in vivo.Surprisingly, cocaine selectively enhanced the DA release from and vesicle replenishment in FRP.Using a cocaine-insensitive DAT knockin mouse, we found that cocaine-facilitated FRP release was mediated by DAT, the same protein for DA reuptake.In contrast, PRP release was selectively modulated by methamphetamine (mAMPH) and D2 receptor.Finally□FRP had a distinct impact on locomotor behaviors.Thus, following cocaine-DAT-binding, DA overflow is enhanced via two distinct pathways: the well-known blockade of DA reuptake, and the novel enhancement of DA release through increasing FRP size and accelerating FRP replenishment in mouse striatum in vivo.
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