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厌恶训练后诱导的岛叶皮质和杏仁核损伤会损害记忆:训练程度的影响。

Insular cortex and amygdala lesions induced after aversive training impair retention: effects of degree of training.

作者信息

Bermúdez-Rattoni F, Introini-Collison I, Coleman-Mesches K, McGaugh J L

机构信息

Departmento de Neurociencias, Instituto de Fisiologia Celular Urtiversidad Nacional Autónoma de México, Mexico City, Mexico.

出版信息

Neurobiol Learn Mem. 1997 Jan;67(1):57-63. doi: 10.1006/nlme.1996.3747.

Abstract

These experiments examined the effects of N-methyl-D-aspartate (NMDA)-induced lesions of the amygdala and insular cortex induced 1 week after rats were trained on a footshock motivated escape task in a two-compartment runway. In the first experiment, male rats were given 10 training trials and, 1 week later, received microinjections of a buffer solution or NMDA into either the insular cortex (IC) or the amygdala (AM). In an inhibitory avoidance retention test 1 week after the microinjections, the retention latencies (i.e., latencies to enter the compartment where shock had been delivered) of both the AM- and "IC-lesioned" groups were significantly lower than those of the buffer-injected groups. Additionally, in comparison with the buffer controls, rats in the two lesioned groups made significantly more crossings between the two compartments during the retention test. In a second experiment, male rats were given 1, 10, or 20 escape training trials 1 week before receiving either sham or NMDA lesions in the IC. The retention test was given 1 week after microinjection. Those sham or lesioned animals that were given only one training trial did not demonstrate retention. Both lesioned groups given 10 or 20 training trials were significantly disrupted on both the step-through latencies, and the number of crossings between the two compartments. The retention-impairing effects of NMDA-induced lesions were slightly attenuated in the group given 20 escape training trials. The findings provide additional evidence that the AM and the IC are involved in regulating the long-term retention of aversively motivated training.

摘要

这些实验研究了在大鼠于双室跑道上接受足部电击诱发的逃避任务训练1周后,N-甲基-D-天冬氨酸(NMDA)诱导的杏仁核和岛叶皮质损伤的影响。在第一个实验中,雄性大鼠接受10次训练试验,1周后,向岛叶皮质(IC)或杏仁核(AM)微量注射缓冲溶液或NMDA。在微量注射1周后的抑制性回避保持测试中,AM损伤组和“IC损伤”组的保持潜伏期(即进入曾施加电击的隔室的潜伏期)均显著低于缓冲液注射组。此外,与缓冲液对照组相比,两个损伤组的大鼠在保持测试期间在两个隔室之间的穿越次数显著更多。在第二个实验中,雄性大鼠在接受IC假损伤或NMDA损伤前1周接受1次、10次或20次逃避训练试验。微量注射1周后进行保持测试。仅接受1次训练试验的假损伤或损伤动物未表现出保持能力。接受10次或20次训练试验的两个损伤组在步通潜伏期和两个隔室之间的穿越次数上均受到显著干扰。在接受20次逃避训练试验的组中,NMDA诱导损伤的保持损害作用略有减弱。这些发现提供了额外的证据,表明杏仁核和岛叶皮质参与调节厌恶动机训练的长期保持。

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