Both Metabotropic Glutamate I and II Receptors Mediate Augmentation of Dopamine Release From the Striatum in Methamphetamine-Sensitized Rats.

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  • Shimazoe Takao
    Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Kyushu University
  • Doi Yukiko
    Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Kyushu University
  • Arai Ikumi
    Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Kyushu University
  • Yoshimatsu Akiko
    Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Kyushu University
  • Fukumoto Takako
    Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Kyushu University
  • Watanabe Shigenori
    Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Kyushu University

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  • Both Metabotropic Glutamate 1 and 2 Receptors Mediate Augmentation of Dopamine Release From the Striatum in Methamphetamine-Sensitized Rats

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Abstract

The role of metabotropic glutamate receptor (mGluR) on dopamine overflow from the striatum was studied in methamphetamine (MAP)-sensitized rats. The increase of dopamine release by MAP was significantly inhibited by perfusion of a mGluR antagonist R,S-α-methyl-4-carboxyphenylglycine. The perfused mGluR agonist 1S,3R-1-aminocyclopentane-1,3-dicarboxylic acid enhanced the dopamine level. The enhancement was significantly attenuated by co-perfusion of a mGluR group I antagonist (S)-4-carboxy-3-hydroxyphenylglycine or a mGluR group II antagonist R,S-α-methyl-4-tetrazolylphenylglycine. These suggest that both mGluR group I and II mediate augmentation of dopamine release in MAP-sensitized rats.

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