[Updated on Apr. 18] Integration of CiNii Articles into CiNii Research

Altered Functional Connectivity of the Orbital Cortex and Striatum Associated with Catalepsy Induced by Dopamine D1 and D2 Antagonists

  • Niu Misaki
    Laboratory of Molecular Neuropharmacology, Graduate School of Pharmaceutical Sciences, Osaka University
  • Kasai Atsushi
    Laboratory of Molecular Neuropharmacology, Graduate School of Pharmaceutical Sciences, Osaka University
  • Seiriki Kaoru
    Laboratory of Molecular Neuropharmacology, Graduate School of Pharmaceutical Sciences, Osaka University Institute for Transdisciplinary Graduate Degree Programs, Osaka University
  • Hayashida Misuzu
    Laboratory of Molecular Neuropharmacology, Graduate School of Pharmaceutical Sciences, Osaka University
  • Tanuma Masato
    Laboratory of Molecular Neuropharmacology, Graduate School of Pharmaceutical Sciences, Osaka University
  • Yokoyama Rei
    Laboratory of Molecular Neuropharmacology, Graduate School of Pharmaceutical Sciences, Osaka University
  • Hirato Yumi
    Laboratory of Molecular Neuropharmacology, Graduate School of Pharmaceutical Sciences, Osaka University
  • Hashimoto Hitoshi
    Laboratory of Molecular Neuropharmacology, Graduate School of Pharmaceutical Sciences, Osaka University Open and Transdisciplinary Research Initiatives, Osaka University Department of Molecular Pharmaceutical Sciences, Graduate School of Medicine, Osaka University Molecular Research Center for Children’s Mental Development, United Graduate School of Child Development, Osaka University, Kanazawa University, Hamamatsu University School of Medicine, Chiba University, and University of Fukui Division of Bioscience, Institute for Datability Science, Osaka University

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Abstract

<p>The dopamine system plays an important role in regulating many brain functions, including the motor function. The blockade of dopamine receptors results in a serious motor dysfunction, such as catalepsy and Parkinsonism. However, the neuronal mechanism underlying the drug-induced motor dysfunction is not well understood. Here, we examine brain-wide activation patterns in Fos-enhanced green fluorescent protein reporter mice that exhibit cataleptic behavior induced by SCH39166, a dopamine D1-like receptor antagonist, and raclopride, a dopamine D2-like receptor antagonist. Support vector classifications showed that the orbital cortex (ORB) and striatum including the caudoputamen (CP) and nucleus accumbens (ACB), prominently contribute to the discrimination between brains of the vehicle-treated and both SCH39166- and raclopride-treated mice. Interregional correlations indicated that the increased functional connectivity of functional networks, including the ORB, CP, and ACB, is the common mechanism underlying SCH39166- and raclopride-induced cataleptic behavior. Moreover, the distinct mechanisms in the SCH39166- and raclopride-induced cataleptic behaviors are the decreased functional connectivity between three areas above and the cortical amygdala, and between three areas above and the anterior cingulate cortex, respectively. Thus, the alterations of functional connectivity in diverse brain regions, including the ORB, provide new insights on the mechanism underlying drug-induced movement disorders.</p>

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