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2
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3
Nitrous oxide-antinociception is mediated by opioid receptors and nitric oxide in the periaqueductal gray region of the midbrain.氧化亚氮的抗伤害感受作用由中脑导水管周围灰质区域的阿片受体和一氧化氮介导。
Eur Neuropsychopharmacol. 2008 Mar;18(3):194-9. doi: 10.1016/j.euroneuro.2007.06.008. Epub 2007 Aug 1.
4
The neural pathway of galanin in the hypothalamic arcuate nucleus of rats: activation of beta-endorphinergic neurons projecting to periaqueductal gray matter.大鼠下丘脑弓状核中甘丙肽的神经通路：投射至导水管周围灰质的β-内啡肽能神经元的激活
J Neurosci Res. 2007 Aug 15;85(11):2400-6. doi: 10.1002/jnr.21396.
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Dynorphin-mediated antinociceptive effects of L-arginine and SIN-1 (an NO donor) in mice.强啡肽介导的L-精氨酸和SIN-1（一种一氧化氮供体）对小鼠的抗伤害感受作用。
Brain Res Bull. 2006 Jul 31;70(3):245-50. doi: 10.1016/j.brainresbull.2006.05.008. Epub 2006 Jun 9.
7
Correlation of inbred mouse sensitivity to nitrous oxide antinociception with brain nitric oxide synthase activity following exposure to nitrous oxide.近亲繁殖小鼠对一氧化二氮抗伤害感受的敏感性与暴露于一氧化二氮后大脑一氧化氮合酶活性的相关性。
Pharmacol Biochem Behav. 2005 Aug;81(4):764-8. doi: 10.1016/j.pbb.2005.05.013.
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Self-administered nitrous oxide for the management of incident pain in terminally ill patients: a blinded case series.自我给药一氧化二氮用于管理晚期患者的突发性疼痛：一项盲法病例系列研究。
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9
An in vivo profile of beta-endorphin release in the arcuate nucleus and nucleus accumbens following exposure to stress or alcohol.暴露于应激或酒精后，弓状核和伏隔核中β-内啡肽释放的体内情况。
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10
Antagonism of nitrous oxide antinociception in mice by antisense oligodeoxynucleotide directed against neuronal nitric oxide synthase enzyme.针对神经元型一氧化氮合酶的反义寡脱氧核苷酸对小鼠一氧化二氮镇痛作用的拮抗作用。
Behav Brain Res. 2004 Jul 9;152(2):361-3. doi: 10.1016/j.bbr.2003.10.019.

一氧化二氮诱导的大鼠弓状核和导水管周围灰质中β-内啡肽的一氧化氮依赖的神经元释放。

Nitrous oxide-induced NO-dependent neuronal release of β-endorphin from the rat arcuate nucleus and periaqueductal gray.

机构信息

Department of Pharmaceutical Sciences, College of Pharmacy, Washington State University, Pullman, WA 99164-6534, USA.

出版信息

Brain Res. 2010 Dec 17;1366:38-43. doi: 10.1016/j.brainres.2010.10.010. Epub 2010 Nov 6.

DOI:10.1016/j.brainres.2010.10.010
PMID:20937263
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2993853/
Abstract

Nitrous oxide (N(2)O)-induced antinociception is thought to result from nitric oxide (NO)-dependent neuronal release of endogenous opioid peptides in the central nervous system. The present study employed microdialysis to determine whether exposure to N(2)O stimulates proopiomelanocortin (POMC) neurons to release β-endorphin in the arcuate nucleus (ARC) of the hypothalamus and the periaqueductal gray (PAG) of the midbrain. Male Sprague-Dawley rats were stereotaxically implanted with microdialysis probes in the ARC or PAG. Exposure to 70% N(2)O significantly increased dialysate levels of oxidation products of NO as well as β-endorphin, compared to levels in fractions collected under room air. These increases in the ARC and PAG were abolished by systemic pretreatment with L-N(G)-nitro arginine methyl ester (L-NAME). These findings suggest an association between increased NO activity and the stimulated release of β-endorphin during exposure of rats to N(2)O.

摘要

一氧化二氮（N(2)O）诱导的镇痛作用被认为是由于中枢神经系统中一氧化氮（NO）依赖性内源性阿片肽释放神经元引起的。本研究采用微透析技术来确定暴露于 N(2)O 是否会刺激促肾上腺皮质激素释放激素（POMC）神经元释放β-内啡肽，从而在下丘脑弓状核（ARC）和中脑导水管周围灰质（PAG）中释放。雄性 Sprague-Dawley 大鼠通过立体定向手术将微透析探针植入 ARC 或 PAG。与在室内空气中收集的分数相比，暴露于 70%的 N(2)O 可显著增加 NO 氧化产物以及β-内啡肽的透析液水平。ARC 和 PAG 中的这些增加被全身预先给予 L-N(G)-硝基精氨酸甲酯（L-NAME）所消除。这些发现表明，在大鼠暴露于 N(2)O 期间，NO 活性的增加与β-内啡肽释放的刺激之间存在关联。