Nicotine attenuates naloxone-induced jumping behaviour in morphine-dependent mice

被引:67
作者
Zarrindast, MR
Farzin, D
机构
[1] Department of Pharmacology, School of Medicine, Tehran Univ. of Medical Sciences, Tehran
[2] Department of Pharmacology, School of Medicine, Tehran Univ. of Medical Sciences, Tehran
关键词
nicotine; morphine; naloxone; acetylcholine receptor antagonist; jumping; (mouse); DOPAMINE D-1 ANTAGONIST; SUBSTANCE-P; PHYSICAL DEPENDENCE; SCH; 23390; RELEASE; BRAIN; RECEPTORS; RAT; WITHDRAWAL; MOUSE;
D O I
10.1016/0014-2999(95)00761-X
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
In the present study the effect of nicotine on naloxone-induced jumping behaviour in morphine-dependent mice was examined. In addition, the modulatory role of dopaminergic, adrenergic and cholinergic mechanisms upon the effect of nicotine were investigated. Animals were rendered dependent on morphine by subcutaneous (s.c.) injections of morphine sulfate 3 times a day for 3 days, and jumping behaviour was induced by intraperitoneal (i.p.) administration of naloxone 2 h after the tenth injection of morphine sulfate on day 4. Nicotine (0.001-2 mg/kg s.c.) caused a significant decrease in withdrawal jumping behaviour in morphine-dependent mice. The effect of nicotine was blocked by the central nicotinic antagonist mecamylamine (0.01-0.1 mg/kg i.p.) but not by the peripheral nicotinic antagonist hexamethonium (0.01 and 0.1 mg/kg i.p.) nor the muscarinic receptor antagonist atropine (2.5-10 mg/kg i.p.). The dopamine receptor antagonist SCH 23390 (R-(+)-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-3-benzazepine-7-ol maleate) (0.01-0.5 mg/kg s.c.) reduced the response induced by nicotine, The dopamine receptor antagonist sulpiride (25 and 50 mg/kg s.c.) and the adrenoceptor antagonists phenoxybenzamine (5 and 10 mg/kg i.p.) and propranolol (5 and 10 mg/kg i.p.) were without an effect. The results indicate that the effect of nicotine on naloxone-induced jumping is mediated by central nicotinic receptors.
引用
收藏
页码:1 / 6
页数:6
相关论文
共 43 条
[31]  
NEAL BS, 1986, J PHARMACOL EXP THER, V236, P157
[32]   EFFECT OF ACUTE AND SUBCHRONIC NICOTINE TREATMENT ON CORTICAL ACETYLCHOLINE-RELEASE AND ON NICOTINIC RECEPTORS IN RATS AND GUINEA-PIGS [J].
NORDBERG, A ;
ROMANELLI, L ;
SUNDWALL, A ;
BIANCHI, C ;
BEANI, L .
BRITISH JOURNAL OF PHARMACOLOGY, 1989, 98 (01) :71-78
[33]   BIPHASIC EFFECTS OF CHRONIC NICOTINE TREATMENT ON HYPOTHALAMIC IMMUNOREACTIVE BETA-ENDORPHIN IN THE MOUSE [J].
ROSECRANS, JA ;
HENDRY, JS ;
HONG, JS .
PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR, 1985, 23 (01) :141-143
[34]  
SAELENS JK, 1971, ARCH INT PHARMACOD T, V190, P213
[35]   CHARACTERIZATION OF CENTRAL NICOTINIC RECEPTORS BY STUDIES ON THE NICOTINE CUE AND CONDITIONED TASTE-AVERSION IN RATS [J].
STOLERMAN, IP .
PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR, 1988, 30 (01) :235-242
[36]   2 DOPAMINE-RECEPTORS - BIOCHEMISTRY, PHYSIOLOGY AND PHARMACOLOGY [J].
STOOF, JC ;
KEBABIAN, JW .
LIFE SCIENCES, 1984, 35 (23) :2281-2296
[37]   INHIBITORY EFFECTS OF GABA, L-GLUTAMIC ACID AND NICOTINE ON THE POTASSIUM-EVOKED RELEASE OF SUBSTANCE-P IN SUBSTANTIA NIGRA SLICES OF THE RAT [J].
TORRENS, Y ;
BEAUJOUAN, JC ;
BESSON, MJ ;
MICHELOT, R ;
GLOWINSKI, J .
EUROPEAN JOURNAL OF PHARMACOLOGY, 1981, 71 (04) :383-392
[38]   EXCESS RELEASE OF SUBSTANCE-P FROM THE SPINAL-CORD OF MICE DURING MORPHINE-WITHDRAWAL AND INVOLVEMENT OF THE ENHANCEMENT OF PRESYNAPTIC CA-2+ ENTRY [J].
UEDA, H ;
TAMURA, S ;
SATOH, M ;
TAKAGI, H .
BRAIN RESEARCH, 1987, 425 (01) :101-105
[39]  
WAY EL, 1969, J PHARMACOL EXP THER, V167, P1
[40]   INVOLVEMENT OF DOPAMINE RECEPTOR SUBTYPES IN MOUSE THERMOREGULATION [J].
ZARRINDAST, MR ;
TABATABAI, SA .
PSYCHOPHARMACOLOGY, 1992, 107 (2-3) :341-346