Effects of repeated administration of a high dose of methamphetamine on dopamine and glutamate release in rat striatum and nucleus accumbens. Brain Res 643: 276-281

Department of Psychiatry and Neurology, Hokkaido University School of Medicine, Sapporo, Japan.
Brain Research (Impact Factor: 2.83). 05/1994; 643(1-2):276-81. DOI: 10.1016/0006-8993(94)90033-7
Source: PubMed

ABSTRACT We examined effects of a high dose of methamphetamine (MA) (4.02 mg free base/kg, s.c., at 2-h intervals, 4 injections) on extracellular concentrations of monoamines such as dopamine (DA), dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), and 5-hydroxyindoleacetic acid (5-HIAA) and those of glutamate and other several amino acids in rat striatum (ST) and nucleus accumbens (NA) using in vivo microdialysis. Five days after the microdialysis, tissue concentrations of monoamines were measured. The toxic dose of MA markedly increased extracellular concentrations of DA, and decreased those of DOPAC, HVA and 5-HIAA in both ST and NA. Magnitude of the increase in DA release was not different between ST and NA. Extracellular concentrations of glutamate showed a gradual increase in ST, but not in NA, while other amino acids showed no changes in both ST and NA. Tissue concentrations of serotonin (5-HT) and 5-HIAA were decreased to 43-58% of control values in both ST and NA, whereas those of DA, DOPAC and HVA showed 43-54% decrease in ST but no changes in NA. These data suggest that the marked increase of DA release is not directly related to the MA-induced dopaminergic neurotoxicity. The increase in glutamate release found only in ST may be related to the dopaminergic damage in ST. It may be that enhanced release in DA and glutamate act synergistically to cause the dopaminergic neurotoxicity in ST. However, enhancement in glutamate release did not appear to be essential for the MA-induced serotonergic neurotoxicity.

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    • "e l s e v i e r . c o m / l o c a t e / s c h r e s afferent transmission of the MPFC to the VTA (Abekawa et al., 1994; Cador et al., 1999; Peterson et al., 2000; Bjijou et al., 2002; Han et al., 2012). Clinical in vivo neuroimaging studies have attempted to add to the pre-clinical (animal) data with respect to the Glu hypothesis, using proton magnetic resonance spectroscopy ( 1 H MRS) in populations of schizophrenia and abstinent METH-addicted adults. "
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    Schizophrenia Research 06/2014; 157(1-3). DOI:10.1016/j.schres.2014.05.004 · 4.43 Impact Factor
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    • "These results were assumed to be caused by the difference between non-specific systemic CPP effects on the entire brain area, and aimed local efficacy in specific brain areas (Wolf, 1998), which was supported by the results of several other studies. For example, a gradual increase in extracellular concentrations of glutamate was found in striatum but not in NAc after a high dose of methamphetamine (Abekawa et al., 1994). An enhanced dopamine and glutamate efflux was also measured by in vivo microdialysis in the prefrontal cortex and striatum in rats sensitized with repeated methamphetamine treatment (Arai et al., 1996; Stephans and Yamamoto, 1995). "
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    European journal of pharmacology 03/2014; DOI:10.1016/j.ejphar.2014.02.028 · 2.68 Impact Factor
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    • "These results suggested that A2a receptors have a protective role in MDMAinduced neural death. Methamphetamine neurotoxicity might also occur via excitotoxic damage following glutamate release and activation of glutamate receptors (Abekawa et al. 1994; Chung et al. 2005; Mark et al. 2004; Marshall et al. 1993). Adenosine exerts potent neuroprotective functions. "
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