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伏隔核壳部损伤会破坏潜伏抑制,但在整个伏隔核损伤后,潜伏抑制会异常持续存在:控制刺激预暴露效应表达和破坏的神经位点。

Latent inhibition is disrupted by nucleus accumbens shell lesion but is abnormally persistent following entire nucleus accumbens lesion: The neural site controlling the expression and disruption of the stimulus preexposure effect.

作者信息

Gal Gilad, Schiller Daniela, Weiner Ina

机构信息

Department of Psychology, Tel-Aviv University, Ramat Aviv, Tel Aviv 69978, Israel.

出版信息

Behav Brain Res. 2005 Jul 30;162(2):246-55. doi: 10.1016/j.bbr.2005.03.019. Epub 2005 Apr 18.

Abstract

Latent inhibition (LI) is the proactive interference of repeated nonreinforced preexposure to a stimulus with subsequent performance on a learning task involving that stimulus. The present experiments investigated the role of the nucleus accumbens (NAC) in LI. LI was measured in a thirst motivated conditioned emotional response procedure with low or high number of conditioning trials, and in two-way active avoidance procedure with the stages of preexposure and conditioning taking place in the same or different contexts. Sham-lesioned rats showed LI with low but not high number of conditioning trials and if preexposure and conditioning took place in the same context but not if the context was changed between the stages. Lesion to the shell subregion of the NAC disrupted LI but LI was preserved in rats with a combined lesion to the NAC shell and core subregions. Moreover, rats with a combined shell-core lesion persisted in showing LI in spite of high number of conditioning trials and in spite of context change. These results show that the NAC is not essential for the acquisition of LI but rather plays a key role in regulating the expression of LI. Moreover, they suggest that the two subregions of the NAC contribute competitively and cooperatively to this process, selecting the response appropriate to the stimulus-no event or the stimulus-reinforcement association in conditioning.

摘要

潜伏抑制(LI)是指对某一刺激的重复非强化预暴露对随后涉及该刺激的学习任务表现产生的前摄干扰。本实验研究了伏隔核(NAC)在潜伏抑制中的作用。在口渴驱动的条件性情绪反应程序中,通过低次数或高次数的条件化试验来测量潜伏抑制,并在双向主动回避程序中,使预暴露和条件化阶段在相同或不同的环境中进行。假手术大鼠在低次数条件化试验时表现出潜伏抑制,但在高次数条件化试验时则没有;并且,如果预暴露和条件化在相同环境中进行,大鼠会表现出潜伏抑制,而如果在两个阶段之间环境发生变化,则不会表现出潜伏抑制。对伏隔核壳部亚区的损伤破坏了潜伏抑制,但在伏隔核壳部和核心亚区联合损伤的大鼠中,潜伏抑制得以保留。此外,如果进行了高次数的条件化试验,或者环境发生了变化,壳 - 核联合损伤的大鼠仍会持续表现出潜伏抑制。这些结果表明,伏隔核对于潜伏抑制的获得并非必不可少,而是在调节潜伏抑制的表达中起关键作用。此外,这些结果还表明,伏隔核的两个亚区在这一过程中既存在竞争性又存在协同性,在条件化过程中选择与刺激 - 无事件或刺激 - 强化关联相适应的反应。

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