Nicotine improvement of Morris water task performance after fimbria-fornix lesion is blocked by mecamylamine

被引:21
作者
Brown, RW [1 ]
Gonzalez, CLR [1 ]
Whishaw, IQ [1 ]
Kolb, B [1 ]
机构
[1] Univ Lethbridge, Dept Psychol & Neurosci, Lethbridge, AB T1K 3M4, Canada
基金
加拿大健康研究院;
关键词
Morris water task; fimbria-fornix lesions; nicotine; mecamylamine; recovery;
D O I
10.1016/S0166-4328(00)00355-7
中图分类号
B84 [心理学]; C [社会科学总论]; Q98 [人类学];
学科分类号
03 ; 0303 ; 030303 ; 04 ; 0402 ;
摘要
The focus of this study was to analyze the effects of nicotine on behavioural compensation after fimbria-fornix (FF) lesions in rats tested on the Morris water task (MWT). Nicotine (0.3 mg/kg) was injected subcutaneously for 11 consecutive days before, for 11 consecutive days after, or for ii consecutive days before and after a FF lesion. Additionally, a lesion group was included that was given mecamylamine (1.0 mg/kg), a nicotine antagonist, 10 min before nicotine administration as well as mecamylamine-only, no treatment lesion, and sham groups. All drug administration ceased 24 h before three consecutive days of behavioural testing on the MWT. Results showed that the sham group and animals receiving both a pre- and post-lesion treatment of nicotine performed significantly better than all other groups, and the pre- and post-lesion nicotine group performed equivalent to sham controls on both acquisition and a probe trial. The compensatory effect of nicotine was blocked by mecamylamine. This study demonstrates that nicotine stimulates recovery from brain damage and the results are discussed in relation to neural mechanisms and potential applications. (C) 2001 Published by Elsevier Science B.V. All rights reserved.
引用
收藏
页码:185 / 192
页数:8
相关论文
共 45 条
[1]   CHRONIC TREATMENTS WITH CHOLINOCEPTOR DRUGS INFLUENCE SPATIAL-LEARNING IN RATS [J].
ABDULLA, FA ;
CALAMINICI, MR ;
STEPHENSON, JD ;
SINDEN, JD .
PSYCHOPHARMACOLOGY, 1993, 111 (04) :508-511
[2]   Relationship between up regulation of nicotine binding sites in rat brain and delayed cognitive enhancement observed after chronic or acute nicotinic receptor stimulation [J].
Abdulla, FA ;
Bradbury, E ;
Calaminici, MR ;
Lippiello, PM ;
Wonnacott, S ;
Gray, JA ;
Sinden, JD .
PSYCHOPHARMACOLOGY, 1996, 124 (04) :323-331
[3]   A COMPARISON OF THE EFFECTS OF ANTERIOR THALAMIC, MAMILLARY BODY AND FORNIX LESIONS ON REINFORCED SPATIAL ALTERNATION [J].
AGGLETON, JP ;
NEAVE, N ;
NAGLE, S ;
HUNT, PR .
BEHAVIOURAL BRAIN RESEARCH, 1995, 68 (01) :91-101
[4]   CIGARETTE-SMOKING AND PARKINSONS-DISEASE [J].
BARON, JA .
NEUROLOGY, 1986, 36 (11) :1490-1496
[5]   D-amphetamine facilitation of Morris water task performance is blocked by eticlopride and correlated with increased dopamine synthesis in the prefrontal cortex [J].
Brown, RW ;
Bardo, MT ;
Mace, DD ;
Phillips, SB ;
Kraemer, PJ .
BEHAVIOURAL BRAIN RESEARCH, 2000, 114 (1-2) :135-143
[6]  
BROWN RW, UNPUB NICOTINE SENSI
[7]  
BROWN RW, PHARM BIOCH BEHAV, V67, P473
[8]   DOPAMINERGIC MECHANISMS IN THE LOCOMOTOR STIMULANT EFFECTS OF NICOTINE [J].
CLARKE, PBS .
BIOCHEMICAL PHARMACOLOGY, 1990, 40 (07) :1427-1432
[9]   DISSOCIATION OF THE APPARENT RELATIONSHIP BETWEEN NICOTINE TOLERANCE AND UP-REGULATION OF NICOTINIC RECEPTORS [J].
COLLINS, AC ;
ROMM, E ;
WEHNER, JM .
BRAIN RESEARCH BULLETIN, 1990, 25 (03) :373-379
[10]   EFFECTS OF NICOTINE ON SPATIAL MEMORY DEFICITS IN RATS WITH SEPTAL-LESIONS [J].
DECKER, MW ;
MAJCHRZAK, MJ ;
ANDERSON, DJ .
BRAIN RESEARCH, 1992, 572 (1-2) :281-285