Intrathecally Administered <sc>D</sc>-Cycloserine Produces Nociceptive Behavior Through the Activation of N-Methyl-<sc>D</sc>-aspartate Receptor Ion-Channel Complex Acting on the Glycine Recognition Site

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  • Tan-No Koichi
    Department of Pharmacology, Tohoku Pharmaceutical University, Japan
  • Esashi Akihisa
    Department of Pharmacology, Tohoku Pharmaceutical University, Japan Department of Pharmacology, School of Medicine, Showa University, Japan
  • Nakagawasai Osamu
    Department of Pharmacology, Tohoku Pharmaceutical University, Japan
  • Niijima Fukie
    Department of Pharmacology, Tohoku Pharmaceutical University, Japan
  • Furuta Seiichi
    Department of Pharmacology and Pharmacotherapy, Nihon Pharmaceutical University, Japan
  • Sato Takumi
    Department of Pharmacology and Pharmacotherapy, Nihon Pharmaceutical University, Japan
  • Satoh Susumu
    Department of Pharmacology and Pharmacotherapy, Nihon Pharmaceutical University, Japan
  • Yasuhara Hajime
    Department of Pharmacology, School of Medicine, Showa University, Japan
  • Tadano Takeshi
    Department of Pharmacology, Tohoku Pharmaceutical University, Japan

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  • Intrathecally administered D-cycloserine produces nociceptive behavior through the activation of N-methyl-D-aspartate receptor ion-channel complex acting on the glycine recognition site
  • Intrathecally administered D‐cycloserine produces nociceptive behavior through the activation of N‐methyl‐d‐aspartate receptor ion‐channel complex acting on the glycine recognition site

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Intrathecal (i.t.) administration of <sc>D</sc>-cycloserine (100 and 300 fmol), a partial agonist of the glycine recognition site on the N-methyl-<sc>D</sc>-aspartate (NMDA) receptor ion-channel complex, produced a behavioral response mainly consisting of biting and/or licking of the hindpaw and the tail along with slight hindlimb scratching directed toward the flank in mice, which peaked at 5 – 10 min and almost disappeared at 15 min after the injection. The behavior induced by <sc>D</sc>-cycloserine (300 fmol) was dose-dependently inhibited by an intraperitoneal injection of morphine (0.5 – 2 mg/kg), suggesting that the behavioral response is related to nociception. The nociceptive behavior was also dose-dependently inhibited by i.t. co-administration of 7-chlorokynurenic acid (0.25 – 4 nmol), a competitive antagonist of the glycine recognition site on the NMDA receptor ion-channel complex; <sc>D</sc>-(−)-2-amino-5-phosphonovaleric acid (62.5 – 500 pmol), a competitive NMDA receptor antagonist; MK-801 (62.5 – 500 pmol), an NMDA ion-channel blocker; ifenprodil (0.5 – 8 nmol); arcaine (31 – 125 pmol); and agmatine (0.1 – 10 pmol), all being antagonists of the polyamine recognition site on the NMDA receptor ion-channel complex. However, [<sc>D</sc>-Phe7,<sc>D</sc>-His9]-substance P(6 – 11), a specific antagonist for substance P (NK1) receptors, and MEN-10,376, a tachykinin NK2-receptor antagonist, had no effect on <sc>D</sc>-cycloserine-induced nociceptive behavior. These results in the mouse spinal cord suggest that <sc>D</sc>-cycloserine-induced nociceptive behavior is mediated through the activation of the NMDA receptor ion-channel complex by acting on the glycine recognition site and that it does not involve the tachykinin receptor mechanism.<br>

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