The dopamine D1 receptor agonist, but not the D2 receptor agonist, induces gene expression of Homer 1a in rat striatum and nucleus accumbens

Hidetaka Yamada, Toshihide Kuroki, Tatsuo Nakahara, Kijiro Hashimoto, Tetsuyuki Tsutsumi, Makoto Hirano, Hisao Maeda

研究成果: ジャーナルへの寄稿学術誌査読

33 被引用数 (Scopus)

抄録

Stimulation of dopamine receptors may induce striatal Homer 1a, an immediate-early gene (IEG) that is involved in the molecular mechanism for the signaling pathway of the group I metabotropic glutamate receptors. This study examined the effects of the agonists for dopamine D1-like and D2-like receptors on gene expression of Homer 1a, in comparison with the IEG c-fos expression, in the discrete brain regions of rats. The D1-like agonist SKF38393 (20 mg/kg, s.c.) significantly increased the mRNA levels of Homer 1a in the striatum and nucleus accumbens, but not in the medial prefrontal cortex or hippocampus, 2 h after injection, whereas the D2-like agonist quinpirole (1 mg/kg, s.c.) had no significant effect on Homer 1a mRNA levels in any brain region examined. Co-administration of SKF38393 and quinpirole significantly increased Homer 1a mRNA levels in the striatum, nucleus accumbens and hippocampus, while this effect was not significantly greater than that of SKF38393 alone. Any treatment did not affect the mRNA levels of other splicing variants, Homer 1b or 1c. In contrast, combination of both dopamine agonists produced a greater increase than SKF38393 did in the mRNA levels of c-fos in the nucleus accumbens, striatum and substantia nigra. These results suggest that stimulation of D1-like receptors, but not D2-like receptors, may induce gene expression of Homer 1a in the striatum and nucleus accumbens. However, in contrast to c-fos expression, it is unlikely that co-activation of both D1-like and D2-like receptors exerts a synergic action on Homer 1a expression in these regions.

本文言語英語
ページ(範囲)88-96
ページ数9
ジャーナルBrain Research
1131
1
DOI
出版ステータス出版済み - 2月 2 2007
外部発表はい

!!!All Science Journal Classification (ASJC) codes

  • 神経科学(全般)
  • 分子生物学
  • 臨床神経学
  • 発生生物学

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