Phenotypic characterization of orofacial movement topography in mutants with disruption of amino acid mechanisms: glutamate N2A/B/D [GluRε1/2/4] subtypes and the GABA synthesizing enzyme GAD65.

@article{Tomiyama2013PhenotypicCO,
  title={Phenotypic characterization of orofacial movement topography in mutants with disruption of amino acid mechanisms: glutamate N2A/B/D [GluRε1/2/4] subtypes and the GABA synthesizing enzyme GAD65.},
  author={Katsunori Tomiyama and Ryoko Ito Kato and Yuko Hara and Masayuki Kobayashi and Masayoshi Mishina and Yuchio Yanagawa and Anthony Kinsella and Noriaki Koshikawa and John L Waddington},
  journal={Neuroscience},
  year={2013},
  volume={250},
  pages={743-54}
}
To investigate the role of glutamate receptor subtypes and GABA in orofacial function, six individual topographies of orofacial movement, both spontaneous and induced by the dopamine D1-like receptor agonist [R/S]-3-methyl-6-chloro-7,8-dihydroxy-1-[3-methyl-phenyl]-2,3,4,5-tetrahydro-1H-3-benzazepine (SKF 83959), were quantified in mutant mice with deletion of (a) GluN2A, B or D receptors, and (b) the GABA synthesizing enzyme, 65-kD isoform of glutamate decarboxylase (GAD65). In GluN2A mutants… CONTINUE READING
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