Dopamine deficiency in mice

Kazuto Kobayashi, Hiromi Sano

研究成果: ジャーナルへの寄稿学術論文査読

16 被引用数 (Scopus)


Dopamine is the principal neurotransmitter that mediates a wide range of brain functions, including locomotion, emotion, learning, and neuroendocrine modulation. To clarify the role of dopamine during postnatal development, it is useful to have mutant mice genetically deleting dopamine. In this paper, we describe the mice lacking expression of tyrosine hydroxylase (TH), the first and rate-limiting enzyme of catecholamine biosynthetic pathway, in the dopaminergic neuronal type. In these mice, TH expression in noradrenergic and adrenergic cells was restored. Lack of TH expression in dopaminergic neurons resulted in a marked reduction of dopamine accumulation. This led to multiple behavioral abnormalities at the juvenile stage, which were characterized by a reduction in spontaneous locomotor activity, blockade of methamphetamine-induced hyperactivity, cataleptic behavior, and defect in active avoidance learning. In contrast, development of pituitary gland as well as production and secretion of the pituitary peptide hormones dependent on hypothalamic dopaminergic control were normally maintained in spite of the reduced dopamine synthesis. Our findings provide genetic evidence that dopamine is essential for controlling spontaneous and voluntary movement and emotional learning during postnatal development through the nigrostriatal and mesocorticolimbic pathways. Copyright (C) 2000 Elsevier Science B.V.

ジャーナルBrain and Development
出版ステータス出版済み - 09-2000

All Science Journal Classification (ASJC) codes

  • 小児科学、周産期医学および子どもの健康
  • 発達神経科学
  • 臨床神経学


「Dopamine deficiency in mice」の研究トピックを掘り下げます。これらがまとまってユニークなフィンガープリントを構成します。