Excessive release of [3H] noradrenaline by veratridine and ischemia in spinal cord

Neurochemistry International
Y SumiyaE S Vizi

Abstract

In this study, the properties of ischemic condition-induced and veratridine-evoked [3H]noradrenaline ([3H]NA) release from rat spinal cord slices were compared. It was expected that ischemia mimicked by oxygen and glucose deprivation results in the impairment of Na+/K+ -ATPase with a consequent elevation of the intracellular Na+ -level which reverses the NA carrier and promotes excessive NA release, and veratridine, by the activation of Na+ channels, releases NA both carrier-mediated and Ca2+ -dependent, i.e. vesicular manner. In our experiments, veratridine (1-100 microM) dose-dependently increased the resting [3H]NA release, and its effect was only partially blocked by low temperature or the lack of external calcium, whereas the sodium channel inhibitor tetrodotoxin (TTX, 1 microM) completely prevented it, indicating that veratridine induces NA release via axonal depolarization and reversing the transporters by eliciting Na+ -influx. In contrast to TTX, the local anesthetic lidocaine (100 microM) only partially blocked the veratridine-induced [3H]NA release due to its inhibitory action on K+ channels. The ischemia-induced [3H]NA release was abolished at 12 degrees C, a temperature known to block only the transporter-mediated ...Continue Reading

References

Feb 1, 1992·Journal of Neurochemistry·V Adam-Vizi
Jan 1, 1997·Brain Research Bulletin·M L KoT Crisp
Jul 4, 1998·European Journal of Pharmacology·Y UchihashiE S Vizi
Jul 9, 1999·Neurochemistry International·E S Vizi, B Sperlágh

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Citations

Nov 13, 2002·Neurochemistry International·Hirotoshi KitagawaKenji Sunagawa
Jan 25, 2005·Autonomic Neuroscience : Basic & Clinical·Eunyoung YiJeffrey A Love
Jun 29, 2018·Acta Pharmacologica Sinica·Xiao-Yu ZhangYe-Hua Gan

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