Nitrous oxide and xenon increase noradrenaline release in the cerebral cortex in vivo and in vitro

Nitrous oxide and xenon increase noradrenaline release in the cerebral cortex in vivo and in vitro
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一氧化二氮和氙增加体内和体外大脑皮层去甲肾上腺素的释放

DOI:
10.1016/j.neulet.2009.11.074
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发表时间:
2010
期刊:
影响因子:
2.5
通讯作者:
Hirota K
Hirota K
中科院分区:
医学4区
文献类型:
--
作者:
Yoshida H;Kushikata T;Tose R;Kudo M;Kudo T;Hirota K

文献摘要

相似文献

去甲肾上腺素在中枢神经系统中起着调节生理功能的重要作用,是全身麻醉的重要机制组成部分。本研究的目的是确定氧化亚氮和氙气是否调节大脑皮层的去甲肾上腺素释放。我们在大鼠身上进行了一系列的体内和体外实验。在体内实验中,在暴露于0、30或60%氧化亚氮的情况下,通过微透析测量前额皮质的去甲肾上腺素释放。在体外实验中,在含Ca2+缓冲液、无Ca2+缓冲液或含Ca2+缓冲液(含10 - 6M河豚毒素(TTX))中,分别用0、15、30或60%氧化亚氮孵育前后,从脑皮质切片中测量去甲肾上腺素的释放。在体内和体外实验中也使用了60%的氙。在体内实验中,暴露于一氧化二氮后,去甲肾上腺素释放浓度呈依赖性增加。在体外实验中,在含Ca2+的条件下,暴露于氧化亚氮期间,脑皮质片的去甲肾上腺素释放以浓度依赖的方式显著增加。在无Ca2+条件下,60%的氧化亚氮产生了显著的去甲肾上腺素释放。在使用和不使用TTX时,一氧化氮增加的去甲肾上腺素释放没有显著差异。氙气也显著增加前额叶皮层和脑皮层切片的去甲肾上腺素释放。氧化亚氮诱导的去甲肾上腺素释放增加可能是由于蓝斑-去甲肾上腺素能神经元的兴奋和其轴突末端的直接刺激。
Noradrenaline in the central nervous system plays an important role in regulating physiological functions, and is a key mechanistic component of general anesthesia. The purpose of this present study was to determine if nitrous oxide and xenon modulate noradrenaline release in the cerebral cortex. We performed a series of in vivo and in vitro experiments in rats. For the in vivo experiments, noradrenaline release was measured by microdialysis in the prefrontal cortex with exposure to 0, 30 or 60% nitrous oxide. For the in vitro experiments, noradrenaline release was measured from cerebrocortical slices before and after incubation with 0, 15, 30, or 60% nitrous oxide in Ca2+-containing buffer, Ca2+-free buffer, or in Ca2+-containing buffer with 10−6M tetrodotoxin (TTX). For the in vivo and in vitro experiments 60% xenon was also used. In the in vivo experiment, following exposure to nitrous oxide, noradrenaline release concentration-dependently increased. In the in vitro experiment, under Ca2+-containing conditions, noradrenaline release from cerebrocortical slices increased significantly during exposure to nitrous oxide in a concentration-dependent manner. Under Ca2+-free conditions, 60% nitrous oxide produced a significant release of noradrenaline. There were no significant differences in nitrous oxide-increased noradrenaline release between with and without TTX. Xenon also significantly increased noradrenaline release in the prefrontal cortex and from the cerebrocortical slices. The nitrous oxide-induced increase in noradrenaline release may be due to both excitation of the locus coeruleus-noradrenergic neuron and direct stimulation of its axon terminals.