Nitric oxide synthase inhibition attenuates tolerance to morphine but not to [D-Ala(2),Glu(4)] deltorphin II, a delta(2)-opioid receptor agonist in mice

被引:26
作者
Zhao, GM [1 ]
Bhargava, HN [1 ]
机构
[1] UNIV ILLINOIS,HLTH SCI CTR,DEPT PHARMACEUT & PHARMACODYNAM,CHICAGO,IL 60612
关键词
morphine; D-Ala(2); Glu(4)]deltorphin II; L-NNA; delta(2)-opioid receptor; analgesia; L-NMMA; tolerance; nitric oxide synthase;
D O I
10.1016/0196-9781(96)00073-3
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The effects of N-G-nitro-L-arginine (L-NNA) and N-G-monomethyl-L-arginine (L-NMMA), two potent inhibitors of nitric oxide synthase (NOS) on the development of tolerance to the analgesic action of [D-Ala(2),Glu(4)]deltorphin II (deltorphin II), a delta(2)-opioid receptor agonist, and morphine, a mu-opioid receptor agonist, were determined in mice. Male Swiss-Webster mice were rendered tolerant to deltorphin II by twice daily ICV injections of the drug for 4 days. Tolerance to morphine was induced by twice daily SC injections of the drug for 4 days. Multiple injections of deltorphin II (20 mu g/mouse) or morphine (15 mg/kg) resulted in the development of tolerance to their analgesic action as evidenced by decreases in the response in comparison to mice injected with vehicle. Concurrent administration of L-NNA or L-NMMA (2, 4, or 8 mg/kg, IP) had no effect on the development of tolerance to the analgesic action of deltorphin II. However, the same doses of L-NNA or L-NMMA inhibited the development of tolerance to the analgesic action of morphine. Acute treatment with L-NNA or L-NMMA did not modify deltorphin II- or morphine-induced analgesia in mice. It is concluded that NOS inhibition attenuates tolerance to the analgesic action of morphine but not to that of deltorphin II, a delta(2)-opioid receptor agonist, in the mouse.
引用
收藏
页码:619 / 623
页数:5
相关论文
共 20 条
[1]   UP-REGULATION OF FOREBRAIN PROENKEPHALIN MESSENGER-RNA SUBSEQUENT TO NMDA RECEPTOR BLOCKADE [J].
ANGULO, JA ;
WATANABE, Y ;
CADET, J ;
LEDOUX, M ;
MCEWEN, BS .
EUROPEAN JOURNAL OF PHARMACOLOGY-MOLECULAR PHARMACOLOGY SECTION, 1993, 244 (03) :317-318
[2]   EFFECT OF OPIOID RECEPTOR AGONISTS ON NITRIC-OXIDE SYNTHASE ACTIVITY IN RAT CEREBRAL-CORTEX HOMOGENATE [J].
BARJAVEL, MJ ;
BHARGAVA, HN .
NEUROSCIENCE LETTERS, 1994, 181 (1-2) :27-30
[3]  
BARJAVEL MJ, 1994, SOC NEUR ABSTR, V20, P234
[4]  
BHARGAVA HN, 1994, PHARMACOL REV, V46, P293
[5]   ATTENUATION OF TOLERANCE TO, AND PHYSICAL-DEPENDENCE ON, MORPHINE IN THE RAT BY INHIBITION OF NITRIC-OXIDE SYNTHASE [J].
BHARGAVA, HN .
GENERAL PHARMACOLOGY, 1995, 26 (05) :1049-1053
[6]   NITRIC-OXIDE SYNTHASE INHIBITION BLOCKS TOLERANCE TO THE ANALGESIC ACTION OF KAPPA-OPIATE RECEPTOR AGONIST IN THE RAT [J].
BHARGAVA, HN .
PHARMACOLOGY, 1994, 48 (04) :234-241
[7]  
BHARGAVA HN, IN PRESS BRAIN RES
[8]   LOCALIZATION OF NITRIC-OXIDE SYNTHASE INDICATING A NEURAL ROLE FOR NITRIC-OXIDE [J].
BREDT, DS ;
HWANG, PM ;
SNYDER, SH .
NATURE, 1990, 347 (6295) :768-770
[9]   NITRIC-OXIDE, A NOVEL NEURONAL MESSENGER [J].
BREDT, DS ;
SNYDER, SH .
NEURON, 1992, 8 (01) :3-11
[10]   GLUTAMATE, NITRIC-OXIDE AND CELL CELL SIGNALING IN THE NERVOUS-SYSTEM [J].
GARTHWAITE, J .
TRENDS IN NEUROSCIENCES, 1991, 14 (02) :60-67