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- W1594196516 abstract "We examined the role of N-methyl-d-aspartate (NMDA) receptors in the control of noradrenaline release in the supraoptic nucleus (SON) using a microdialysis method in urethane-anaesthetized rats. Local application of 0.5 mm NMDA into the SON by retrodialysis decreased noradrenaline content in the dialysate from the SON. On the other hand, MK-801, a channel blocker of NMDA receptors, or D(–)2-amino-5-phosphonopentanoic acid (AP-5), a competitive NMDA receptor antagonist, increased the basal noradrenaline content. Tetrodotoxin did not completely block the noradrenaline increase after NMDA antagonists. Infusion of Ca2+-free solution containing Ni2+ and Cd2+, or a mixture of ω-agatoxin IVA and ω-conotoxin GVIA, voltage-sensitive Ca2+ channels blockers, did not block noradrenaline increase after AP-5, but blocked noradrenaline increase after high K+. Infusion of intracellular Ca2+ blockers, thapsigargin or TMB-8, impaired noradrenaline increase after AP-5 but not that after high K+. These data are consistent with the hypothesis that activation of an NMDA receptor inhibits an intracellular Ca2+ store-dependent noradrenaline release from nerve terminals in the SON." @default.
- W1594196516 created "2016-06-24" @default.
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- W1594196516 date "2001-10-01" @default.
- W1594196516 modified "2023-10-18" @default.
- W1594196516 title "Facilitation of Ca2+Store-Dependent Noradrenaline Release After anN-Methyl-d-Aspartate Receptor Antagonist in the Rat Supraoptic Nucleus" @default.
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- W1594196516 doi "https://doi.org/10.1046/j.1365-2826.2001.00711.x" @default.
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