Premium
Changes in the Neuronal Glutamate Transporter EAAT 3 in Rat Brain after Exposure to Methamphetamine
Author(s) -
Kerdsan Walailuk,
Thanoi Samur,
NudmamudThanoi Sutisa
Publication year - 2012
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/j.1742-7843.2012.00899.x
Subject(s) - glutamatergic , methamphetamine , striatum , meth , glutamate receptor , hippocampus , hippocampal formation , medicine , neuroscience , cortex (anatomy) , neurotransmission , pharmacology , endocrinology , chemistry , biology , dopamine , receptor , monomer , organic chemistry , acrylate , polymer
Methamphetamine ( METH ), an addictive psychostimulant, can induce glutamate release in several brain areas such as cerebral cortex, hippocampus and striatum. Excess glutamate is ordinarily removed from the synaptic cleft by glutamate transporters for maintaining homoeostasis. EAAT 3, a subtype of glutamate transporter expressed mainly by neurons, is a major glutamate transporter in the hippocampus and cortex. Therefore, this study examined the effects of acute and sub‐acute METH administration on the expression of the EAAT 3 in the hippocampal formation, striatum and frontal cortex. Male S prague– D awley rats received vehicle injections (i.p.) for 13 days followed by one injection of METH (8 mg/kg, i.p.) on day 14 in acute group. Animals received METH (4 mg/kg, i.p.) or vehicle for 14 days in sub‐acute and control groups, respectively. EAAT 3 immunoreactivity was determined by western blotting followed by measurement of the integrated optical density. A significant increase in EAAT 3 was found in the hippocampal formation after sub‐acute, but not acute, METH administration. Conversely, a significant decrease in EAAT 3 in striatum was observed in both acute and sub‐acute groups. A trend towards a decrease in EAAT 3 was also found in frontal cortex in the sub‐acute group. Our results of decreased EAAT 3 in striatum and frontal cortex suggest deficits of cortico‐striatal glutamatergic synapses after METH exposure. Increased EAAT 3 expression in the hippocampus may be a compensatory response to possible deficits of glutamatergic neurotransmission induced by METH . Moreover, our findings provide further support for glutamatergic dysfunction with abnormalities involving a transporter important in the regulation of neuronal glutamate.