Increased training in an aversively motivated task attenuates the memory-impairing effects of posttraining N-methyl-D-aspartate-induced amygdala lesions.

Increased training in an aversively motivated task attenuates the memory-impairing effects of posttraining N-methyl-D-aspartate-induced amygdala lesions.
复制标题

增加厌恶动机任务的训练可以减轻训练后 N-甲基-D-天冬氨酸诱发的杏仁核损伤的记忆损伤效应。

DOI:
10.1037//0735-7044.106.5.789
复制
发表时间:
1992
影响因子:
1.9
通讯作者:
McGaugh,JL
McGaugh,JL
中科院分区:
医学4区
文献类型:
--
作者:
Parent,MB;Tomaz,C;McGaugh,JL

文献摘要

被引文献

相似文献

本研究旨在检查术前训练量的变化对训练后杏仁核复合体(AC)病变产生的保留缺陷的影响。大鼠在接受n -甲基- d -天冬氨酸损伤前7天接受了1、10或20次足震刺激逃避任务训练试验。术后4天测量的抑制性回避保留性能表明,增加训练可以改善AC损伤动物和对照动物的保留。与对照组相比,ac损伤动物的保持能力下降;然而,通过增加术前训练,损伤部分减轻。研究发现,与未受损的对照组相比,ac损伤的动物在保留测试中表现出更大的运动活动,这表明活动的增加可能导致抑制回避保留性能受损。保留实验两天后,一些ac损伤的动物随后在同一装置中进行连续多次抑制回避反应训练。交流损伤不妨碍任务的习得或保留。这些发现表明,杏仁核可能不是基于广泛训练介导刺激-影响关联的永久性变化的关键部位。
This study was designed to examine the effect of variations in the amount of preoperative training on the retention deficit produced by posttraining lesions of the amygdaloid complex (AC). Rats received 1, 10, or 20 training trials in a footshock-motivated escape task 7 days before receiving N-Methyl-D-aspartate lesions of the AC. Inhibitory avoidance retention performance, which was measured 4 days postoperatively, indicated that increased training improved retention in AC-lesioned animals as well as in control animals. The retention performance of AC-lesioned animals was impaired when compared with that of controls; however, the impairment was partially attenuated by increased preoperative training. The finding that AC-lesioned animals displayed greater locomotor activity on the retention test compared with nonlesioned controls suggests that the increased activity may have contributed to the impaired inhibitory avoidance retention performance. Two days after the retention test, some of the AC-lesioned animals were subsequently trained on a continuous multiple-trial inhibitory avoidance response in the same apparatus. AC lesions did not block acquisition or retention of the task. These findings suggest that the amygdala may not be a critical site for the permanent changes mediating stimulus–affect associations based on extensive training.