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本文引用的文献

1
Transcriptional and epigenetic mechanisms of addiction.成瘾的转录和表观遗传机制。
Nat Rev Neurosci. 2011 Oct 12;12(11):623-37. doi: 10.1038/nrn3111.
2
Acetaminophen modulation of hydrocodone reward in rats.对乙酰氨基酚对氢可酮奖赏效应的调制作用在大鼠中的研究。
Pharmacol Biochem Behav. 2011 Sep;99(3):307-10. doi: 10.1016/j.pbb.2011.05.003. Epub 2011 May 11.
3
Overprescription of postoperative narcotics: a look at postoperative pain medication delivery, consumption and disposal in urological practice.术后麻醉药物的过度处方:泌尿科术后疼痛药物管理、使用和处置情况分析。
J Urol. 2011 Feb;185(2):551-5. doi: 10.1016/j.juro.2010.09.088. Epub 2010 Dec 18.
4
Modulation of opiate-related signaling molecules in morphine-dependent conditioned behavior: conditioned place preference to morphine induces CREB phosphorylation.吗啡依赖条件行为中阿片相关信号分子的调制:吗啡条件性位置偏爱诱导 CREB 磷酸化。
Neuropsychopharmacology. 2010 Mar;35(4):955-66. doi: 10.1038/npp.2009.199. Epub 2009 Dec 2.
5
Comparison of the antinociceptive response to morphine and morphine-like compounds in male and female Sprague-Dawley rats.雄性和雌性斯普拉格-道利大鼠对吗啡及吗啡样化合物的抗伤害感受反应比较。
J Pharmacol Exp Ther. 2006 Mar;316(3):1195-201. doi: 10.1124/jpet.105.094276. Epub 2005 Nov 16.
6
A preclinical comparison between different opioids: antinociceptive versus adverse effects.不同阿片类药物之间的临床前比较:镇痛作用与不良反应
Pharmacol Biochem Behav. 2005 Feb;80(2):309-26. doi: 10.1016/j.pbb.2004.12.002. Epub 2005 Jan 7.
7
Addictive and non-addictive drugs induce distinct and specific patterns of ERK activation in mouse brain.成瘾性药物和非成瘾性药物在小鼠大脑中诱导出不同且特定的细胞外信号调节激酶(ERK)激活模式。
Eur J Neurosci. 2004 Apr;19(7):1826-36. doi: 10.1111/j.1460-9568.2004.03278.x.
8
In vivo regulation of extracellular signal-regulated protein kinase (ERK) and protein kinase B (Akt) phosphorylation by acute and chronic morphine.急性和慢性吗啡对细胞外信号调节蛋白激酶(ERK)和蛋白激酶B(Akt)磷酸化的体内调节
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9
Brain region-specific mechanisms for acute morphine-induced mitogen-activated protein kinase modulation and distinct patterns of activation during analgesic tolerance and locomotor sensitization.急性吗啡诱导的丝裂原活化蛋白激酶调节的脑区特异性机制以及镇痛耐受和运动敏化过程中不同的激活模式。
J Neurosci. 2003 Sep 10;23(23):8360-9. doi: 10.1523/JNEUROSCI.23-23-08360.2003.

氢可酮和吗啡具有相似的奖赏效应,并减少伏隔核中 ERK 和 CREB 的磷酸化。

Hydrocodone and morphine possess similar rewarding effects and reduce ERK and CREB phosphorylation in the nucleus accumbens.

机构信息

Department of Pharmaceutical Sciences, Western University of Health Sciences, Pomona, California 91766, USA.

出版信息

Synapse. 2012 Oct;66(10):918-22. doi: 10.1002/syn.21577. Epub 2012 Jul 2.

DOI:10.1002/syn.21577
PMID:22715022
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3418391/
Abstract

The number of prescriptions for hydrocodone-containing opioid analgesics has greatly increased over the past decade. This increase has led to an associated enhancement in the nonmedical use of hydrocodone products. There is a lack of evidence to determine the extent of the rewarding effects and signal transduction properties of hydrocodone. Therefore, this study aimed to examine the rewarding properties of hydrocodone (1 and 5 mg/kg) and morphine (1 and 5 mg/kg) using the conditioned place preference paradigm (CPP) in rats. Both hydrocodone and morphine produced a CPP at the 5 mg/kg dose, but not the lower 1 mg/kg dose, suggesting that both drugs possess similar rewarding properties in the CPP paradigm. Moreover, hydrocodone and morphine equally reduced phosphorylation levels of ERK and CREB proteins in the nucleus accumbens, suggesting that both drugs exert their effects through signal transduction pathways known to be involved in drug reward and reinforcement. These findings suggest that hydrocodone should be viewed as similarly capable of producing rewarding and euphoric properties as morphine.

摘要

在过去的十年中,含有氢可酮的阿片类镇痛药的处方数量大大增加。这种增加导致了氢可酮产品的非医疗用途的相应增强。目前缺乏证据来确定氢可酮的奖赏效应和信号转导特性的程度。因此,本研究旨在使用大鼠条件性位置偏爱范式(CPP)来检查氢可酮(1 和 5mg/kg)和吗啡(1 和 5mg/kg)的奖赏特性。氢可酮和吗啡都在 5mg/kg 剂量下产生 CPP,但在较低的 1mg/kg 剂量下没有产生 CPP,这表明这两种药物在 CPP 范式中具有相似的奖赏特性。此外,氢可酮和吗啡同样降低了伏隔核中 ERK 和 CREB 蛋白的磷酸化水平,这表明这两种药物通过已知参与药物奖赏和强化的信号转导途径发挥作用。这些发现表明,氢可酮应该被视为与吗啡一样能够产生奖赏和欣快特性。