Methamphetamine-induced dopamine transporter complex formation and dopaminergic deficits: the role of D2 receptor activation.

ABSTRACT: Methamphetamine (METH) abuse is a serious public health issue. Of particular concern are findings that repeated high-dose administrations of METH cause persistent dopaminergic deficits in rodents, nonhuman primates, and humans. Previous studies have also revealed that METH treatment causes alterations in the dopamine transporter (DAT), including the formation of higher molecular mass DAT-associated complexes. The current study extends these findings by examining mechanisms underlying DAT complex formation. The association among DAT complex formation and other METH-induced phenomena, including alterations in vesicular monoamine transporter 2 (VMAT2) immunoreactivity, astrocytic activation [as assessed by increased glial fibrillary acidic protein (GFAP) immunoreactivity], and persistent dopa

SUBMITTER: Hadlock GC 

PROVIDER: S-EPMC2957782 | biostudies-literature | 2010 Oct

REPOSITORIES: biostudies-literature