Functional role of postsynaptic dopamine receptors in substantia gelatinosa neurons of the spinal cord

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  • Nakatsuka Terumasa
    Department of Physiology, Faculty of Medicine, Saga University
  • Tamae Akihiro
    Department of Integrative Physiology, Graduate School of Medical Sciences, Kyushu University
  • Koga Kohei
    Department of Integrative Physiology, Graduate School of Medical Sciences, Kyushu University
  • Kato Go
    Department of Integrative Physiology, Graduate School of Medical Sciences, Kyushu University
  • Fujita Tsugumi
    Department of Physiology, Faculty of Medicine, Saga University
  • Furue Hidemasa
    Department of Integrative Physiology, Graduate School of Medical Sciences, Kyushu University
  • Kumamoto Eiichi
    Department of Physiology, Faculty of Medicine, Saga University
  • Yoshimura Megumu
    Department of Integrative Physiology, Graduate School of Medical Sciences, Kyushu University

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Other Title
  • 脊髄膠様質細胞におけるシナプス後細胞ドーパミン受容体の機能的意義

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Abstract

   Dopamine (DA) is the most abundant catecholamine in the brain. The important contribution of DA as a neurotransmitter in the brain is well understood. Compared with the enormous literature devoted to DA actions in the brain, little is known about the roles of DA in the spinal cord. Dopaminergic innervation of the spinal cord is largely derived from cerebral structures. The periventricular, posterior (A11) region of the hypothalamus is the principle source of descending dopaminergic pathways. To understand the mechanisms of antinociception mediated by the descending dopaminergic pathway, we examined the actions of DA on nociceptive transmission using whole-cell patch-clamp recordings from substantia gelatinosa (SG) neurons in spinal cord slices. Bath application of DA produced an outward current in almost all SG neurons examined. The DA-induced outward current was blocked by the addition of K+-channel blockers (Cs+ and TEA) or GDP-β-S into pipette solution, and was reduced in the presence of Ba2+. The DA-induced outward current was mimicked by a D2-like receptor agonist, quinpirole, but not by a D1-like receptor agonist, SKF 38393. In addition, the DA-induced outward current was suppressed by a D2-like receptor antagonist, sulpiride, but not by a D1-like receptor antagonist, SCH 23390. These results indicate that DA acts on postsynaptic SG neurons to induce an outward current by G-proteinmediated activation of K+ channels through D2-like receptors. This may be a possible mechanism for antinociception by the descending dopaminergic pathway.

Journal

  • PAIN RESEARCH

    PAIN RESEARCH 20 (3), 105-110, 2005

    JAPANESE ASSOCIATION FOR STUDY OF PAIN

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