Catecholaminergic signaling regulates various physiological functions,
such as blood pressure1 and is implicated in drug dependence,
affective disorders and male aggressive behavior2,
3. The actions
of released catecholamines are terminated by sodium-driven, high-affinity
transporters in the plasma membrane of the releasing neurons4,
5
and by a corticosterone-sensitive, low-affinity, high-capacity extraneuronal
transport system6, originally named uptake2, found
in sympathetically innervated tissues7 and in central nervous
system glia8. Here we report the molecular identification and
pharmacological characterization of the extraneuronal catecholamine transporter,
which is unrelated to the family of sodium-driven neuronal monoamine transporters5.
