笑気鎮痛における脊髄 Ca^<2+> チャネルおよび細胞内情報伝達系の関与

概要

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Nitrous oxide (N_2O) has a potent antinociceptive action, The spinal Ca^<2+> channel and the intracellular signal transducing system have recently been suggested to play an important role in pain transmission and modulation. The present study was undertaken to evaluate further the involvement of the Ca^<2+> channels and the intracellular signal transducing system activity in N_2O analgesia by investigating tail-flick latency and in vitro autoradiography. Wister rats were exposed to either 70% N_2 (control) or 70% N_2O with 30% O_2 for 2 hours after staying 30 minutes in plastic box. N_2O produced analgesia : the percent maximal effect (%MPE ; tail-flick latency) increased to 79% at 30 minutes after starting of N_2O inhalation. At the end of N_2O exposure, ^<125>I-ωCgTx binding (N type Ca^<2+> channel activity) in the spiral cord (Rexed I-II) decreased by 20% accompanied by a decreased in ^3H-forskolin binding (adenylate cyclase : 22%), while ^3H-PN 200-110 binding (L type Ca^<2+> channel activity) and ^3H-GTP binding (G-protein) did not changed. These results suggest that the interactions with N type Ca^<2+> channel and adenylate cyclase in the dorsal horn of the spiral cord are involved in analgesia induced by N_2O inhalation.
2000-06-25