Mice lacking rhes show altered morphine analgesia, tolerance, and dependence

被引：10
作者：
Lee, Franklin A. [2 ]
Baiamonte, Brandon A. [2 ]
Spano, Daniela [3 ]
LaHoste, Gerald J. [2 ]
Soignier, R. Denis [2 ]
Harrison, Laura M. [1 ]
机构：
[1] Louisiana State Univ, Hlth Sci Ctr, Neurosci Ctr Excellence, New Orleans, LA 70112 USA
[2] Univ New Orleans, Dept Psychol, New Orleans, LA 70148 USA
[3] Univ Naples Federico II, Dipartimento Biochim & Biotecnol Med, Naples, Italy
来源：
NEUROSCIENCE LETTERS | 2011年 / 489卷 / 03期
基金：
美国国家卫生研究院;
关键词：
RASD2; Opioid; Tolerance; Analgesia; Dependence; GTP-binding protein; GTP-BINDING PROTEIN; ADENYLYL-CYCLASE; SIGNAL-TRANSDUCTION; PHOSPHOLIPASE-C; MUTANT MICE; RECEPTOR; DOPAMINE; STRIATUM; RAT; HYPERALGESIA;
D O I：
10.1016/j.neulet.2010.12.012
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
Rhes, the Ras Homolog Enriched in Striatum, is an intermediate-size GTP binding protein. Although its full functions are not yet known, it has been shown to affect signaling and behaviors mediated by G protein-coupled receptors. Here we have tested whether Rhes affects behaviors mediated by opioid receptors. Wild type and rhes-deficient mice were administered morphine and tested for analgesia in formalin and tail flick tests. Rhes(-/-) mice showed significantly enhanced analgesia in both tests relative to rhes(+/+) mice. Furthermore, rhes(-/-) mice did not display tolerance to repeated morphine administration and displayed significantly less withdrawal than rhes(+/+) mice. These findings indicate that Rhes is involved in behaviors mediated by mu opioid receptors and in the adaptive response to repeated morphine administration. (C) 2010 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码：182 / 186
页数：5
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