Exposure to nitrous oxide stimulates a nitric oxide-dependent neuronal release of beta-endorphin in ventricular-cisternally-perfused rats.
Exposure to nitrous oxide stimulates a nitric oxide-dependent neuronal release of beta-endorphin in ventricular-cisternally-perfused rats.
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DOI：
10.1016/j.brainres.2009.08.091
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发表时间：
2009-12-01
期刊：
影响因子：
2.9
通讯作者：
Quock, Raymond M.
中科院分区：
文献类型：
--
作者：
Zelinski, Lisa M.;Ohgami, Yusuke;Quock, Raymond M.
我们以前已经证明，在大鼠热板试验中，一氧化二氮（N2 O）的抗伤害效应对内源性阿片肽β-内啡肽抗血清的拮抗作用敏感。此外，N2 O诱导的抗伤害感受通过抑制脑中一氧化氮（NO）的产生而降低。为了验证N_2O可能刺激NO依赖的神经元释放β-内啡肽的假设，我们在麻醉的Sprague道利大鼠中进行了人工脑脊液（aCSF）的脑室-脑池灌注。从单独的暴露于室内空气的大鼠、暴露于N2 O的大鼠和L-NAME预处理的N2 O暴露的大鼠组中收集10分钟的aCSF灌流液组分;然后分析它们的NO代谢物和β-内啡肽含量。与室内空气对照相比，暴露于70%N2O增加了NO代谢产物亚硝酸盐和硝酸盐以及β-内啡肽的灌流液水平。用NO合成酶抑制剂L-NG-硝基精氨酸甲酯预处理大鼠，可防止N_2O引起的亚硝酸盐、硝酸盐和β-内啡肽的增加。这些发现表明，在体内大鼠模型中，N2 O可以刺激NO依赖性神经元释放β-内啡肽。
We have previously shown that the antinociceptive effect of nitrous oxide (N2O) in the rat hot plate test is sensitive to antagonism by antisera against the endogenous opioid peptide β-endorphin. Moreover, N2O-induced antinociception is reduced by inhibition of nitric oxide (NO) production in the brain. To test the hypothesis that N2O might stimulate an NO-dependent neuronal release of β-endorphin, we conducted a ventricular-cisternal perfusion with artificial cerebrospinal fluid (aCSF) in urethane-anesthetized Sprague Dawley rats. Ten-min fractions of aCSF perfusate were collected from separate groups of room air-exposed rats, N2O-exposed rats, and L-NAME-pretreated, N2O-exposed rats; they were then analyzed for their content of NO metabolites and β-endorphin. Compared to room air control, exposure to 70% N2O increased perfusate levels of the NO metabolites nitrite and nitrate as well as β-endorphin. Pretreatment of rats with L-NG-nitro arginine methyl ester, an inhibitor of NO synthase, prevented the N2O-induced increases in nitrite, nitrate and β-endorphin. These findings demonstrate in an in vivo rat model that N2O may stimulate an NO-dependent neuronal release of β-endorphin.
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影响因子：
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