Amphetamine administration does not alter protein levels of the GLT-1 and EAAC1 glutamate transporter subtypes in rat midbrain, nucleus accumbens, striatum, or prefrontal cortex

Our laboratory and others have previously shown that glutamate transmission is required for chronic amphetamine-induced neuroadaptations, and that glutamate transmission itself is altered by chronic amphetamine administration. For example, N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) receptor subunit expression are altered in a region- and withdrawal-specific manner. The goal of this study was to determine whether repeated amphetamine administration influences the expression of two glutamate transporter subtypes, GLT-1 and EAAC1. Rats were treated with saline or 5 mg/kg amphetamine for 5 days (chronic saline and amphetamine groups, respectively), or saline for 4 days and 5 mg/kg amphetamine on day 5 (acute amphetamine group), and decapitated 24 h after the last injection. Tissue was dissected from brain regions involved in the psychomotor effects of amphetamine (nucleus accumbens, striatum, prefrontal cortex, ventral tegmental area, and substantia nigra). Levels of GLT-1 and EAAC1 were quantified by Western blotting and normalized to actin levels. We found no significant change in levels of GLT-1 or EAAC1 in response to either acute or chronic amphetamine treatment. These findings suggest that the transporter component of the glutamate system might not play a significant role in the alterations in glutamate transmission observed following repeated amphetamine administration.