Stimulatory Effect of Endothelin-1 on Neurons in the Nucleus Tractus Solitarii Is Mediated by Non-N-Methyl-D-Aspartate Receptors.

  • SHIHARA Miwako
    Department of Cardiovascular Medicine, Cardiovascular Science, Graduate School of Medical Sciences, Kyushu University
  • HIROOKA Yoshitaka
    Department of Cardiovascular Medicine, Cardiovascular Science, Graduate School of Medical Sciences, Kyushu University
  • ESHIMA Kenichi
    Department of Cardiovascular Medicine, Cardiovascular Science, Graduate School of Medical Sciences, Kyushu University
  • HORI Nobuaki
    Department of Pharmacology, Kyushu University School of Dentistry
  • TAKESHITA Akira
    Department of Cardiovascular Medicine, Cardiovascular Science, Graduate School of Medical Sciences, Kyushu University

この論文をさがす

抄録

We previously demonstrated that endothlin-1 (ET-1) augments and ETA receptor antagonist attenuates excitatory neuronal response to glutamate (Glu) in brainstem slices from normotensive rats. The aim of this study was to determine which type of Glu receptor is responsible for the stimulatory effects of ET-1 on neurons of the nucleus tractus solitarii (NTS). Single unit discharges were recorded extracellularly from rat brainstem slice preparations. Seven NTS neurons that were excited by solitary tract (ST) stimulation responded to iontophoretically applied ET-1 with neuronal activity. An N-methyl-D-aspartate (NMDA) receptor antagonist, non-NMDA, 6-cyano-7-nitro-quinoxaline-2, 3-dione (CNQX), or DL-2-amino-5-phosphonovaleric acid (AP-5) was perfused over the slices with Kreb’s-Ringer solution. The increase in neuronal activity evoked by iontophoretically applied ET-1 was nearly abolished by CNQX but not by AP-5. CNQX but not AP-5 decreased the basal spontaneous neuronal activity of NTS neurons. These results suggest that non-NMDA receptors play a role in mediating the stimulatory effect of ET-1 on neuronal activity in the NTS. (Hypertens Res 2001; 24: 137-142)

収録刊行物

被引用文献 (2)*注記

もっと見る

参考文献 (51)*注記

もっと見る

詳細情報 詳細情報について

問題の指摘

ページトップへ