Simple and configural association learning in rats with bilateral quisqualic acid lesions of the nucleus basalis magnocellularis

被引:18
作者
Butt, AE [1 ]
Hodge, GK
机构
[1] Univ New Mexico, Dept Psychol, Albuquerque, NM 87131 USA
[2] Univ Montreal, Dept Physiol, Montreal, PQ H3C 3J7, Canada
关键词
acetylcholine; cholinergic; Alzheimer's disease; configural association theory; basal forebrain; memory;
D O I
10.1016/S0166-4328(97)00062-4
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
We hypothesized that bilateral quisqualic acid lesions of the nucleus basalis magnocellularis (NBM) in rats would impair configural but not simple association learning. In experiment 1, rats were tested in a negative patterning operant discrimination where they were food-reinforced for responding to a light or a tone (L+, T+) but not for responding to the configural stimulus consisting of the light and tone presented simultaneously (LT-). Consistent with our hypothesis, NBM-lesioned rats showed a transient but significant impairment, responding normally to L+ and T+ but responding more often to LT-, in addition to responding more often during the inter-trial interval (ITI) than controls. In experiment 2, rats were tested in a simple operant discrimination where rats were food-reinforced for responding to a light (L+) but not for responding to a tone (T-). Although NBM-lesioned rats again responded normally to L+ as predicted, NBM-lesioned rats were transiently impaired, making more T- responses and more ITI responses than controls. Together, these results suggest that the NBM is involved in both configural and simple association learning but that this involvement is limited to learning to withhold responding to non-reinforced contextual or discrete stimuli. Finally, rats from experiment 2 underwent extinction trials, where results showed no difference between NBM-lesioned and control groups, suggesting that the NBM is not involved in the extinction of conditioned responding to previously reinforced stimuli. (C) 1997 Elsevier Science B.V.
引用
收藏
页码:71 / 85
页数:15
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