POST-TRAINING DOWN-REGULATION OF MEMORY CONSOLIDATION BY A GABA-A MECHANISM IN THE AMYGDALA MODULATED BY ENDOGENOUS BENZODIAZEPINES

被引:52
作者
IZQUIERDO, I [1 ]
DA CUNHA, C [1 ]
HUANG, CH [1 ]
WALZ, R [1 ]
WOLFMAN, C [1 ]
MEDINA, JH [1 ]
机构
[1] UNIV BUENOS AIRES, FAC MED, INST BIOL CELULAR, NEURORECEPTORES LAB, RA-1113 BUENOS AIRES, ARGENTINA
来源
BEHAVIORAL AND NEURAL BIOLOGY | 1990年 / 54卷 / 02期
关键词
D O I
10.1016/0163-1047(90)91282-G
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
In rats, amygdala benzodiazepine-like immunoreactivity decreases by 29% immediately after the animals step down from the platform of an inhibitory avoidance apparatus and decreases by a further 45% immediately after they receive a training footshock. The decrease is attributable to a release of diazepam or diazepam-like molecules. The immediate post-training intraamygdala injection of the central benzodiazepine antagonist flumazenil (10 nmole/amygdala) causes memory facilitation, and that of the GABA-A agonist muscimol (0.005 to 0.5 nmole) causes retrograde amnesia. Pretraining ip flumazenil administration (2.0 and 5.0 mg/kg) attenuates the effect of post-training muscimol by a factor of at least 100. The higher dose of pretraining flumazenil also causes memory facilitation. The data suggest that post-training consolidation is down-regulated by a GABA-A mechanism in the amygdala modulated by endogenous benzodiazepines released during training and at the time of consolidation. © 1990 Academic Press, Inc.
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收藏
页码:105 / 109
页数:5
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