Differential fear conditioning induces reciprocal changes in the sensory responses of lateral amygdala neurons to the CS+ and CS-

Differential fear conditioning induces reciprocal changes in the sensory responses of lateral amygdala neurons to the CS+ and CS-
复制标题

DOI:
10.1101/lm.7.2.97
复制
发表时间:
2000-03-01
期刊:
影响因子:
2
通讯作者:
Paré, D
Paré, D
中科院分区:
医学4区
文献类型:
--
作者:
Collins, DR;Paré, D

文献摘要

被引文献

相似文献

在经典的恐惧条件反射中,中性感觉刺激(CS)在与有害的无条件刺激(US)配对后获得诱发恐惧反应的能力。由于杏仁核损伤阻止恐惧反应的获得,而杏仁外侧核(LA)是杏仁核听觉传出的主要输入站,因此,我们研究了听觉恐惧条件反射对LA神经元感觉反应的影响。尽管条件反射显示能增加CS诱发的促黄体生成素反应,但这种反应性改变的特异性并未得到检验。因为条件反射可能会导致LA对听觉传入反应的非特异性增加,我们在清醒的、头约束的汽车中重新研究了这个问题,使用了一种差异条件反射范式,其中只有两个音调中的一个(CS+而不是CS-)与US配对。差异条件反射增加了对CS+的单位和场反应,而降低了对CS-的反应。这种变化从未在杏仁核中观察到,除非之前CS-曾与美国配对,并且恐惧反应没有消失。这表明,恐惧条件反射不仅伴随着传递CS+的杏仁顶叶通路的增强,而且还伴随着对伤害性刺激不成对的感觉输入的抑制。
In classical fear conditioning, a neutral sensory stimulus (CS) acquires the ability to elicit fear responses after pairing to a noxious unconditioned stimulus (US). As amygdala lesions prevent the acquisition of fear responses and the lateral amygdaloid (LA) nucleus is the main input station of the amygdala for auditory efferents, the effect of auditory fear conditioning on the sensory responsiveness of LA neurons has been examined. Although conditioning was shown to increase CS-evoked Lh responses, the specificity of the changes in responsiveness was not tested. Because conditioning might induce nonspecific increases in LA responses to auditory afferents, we re-examined this issue in conscious, head-restrained cars using a differential conditioning paradigm where only one of two tones (CS+ but not CS-) was paired to the US. Differential conditioning increased unit and field responses to the CS+, whereas responses to the CS- decreased. Such changes have never been observed in the amygdala except in cases where the CS- had been paired to the US before and fear responses not extinguished. This suggests that fear conditioning is not only accompanied by potentiation of amygdalopetal pathways conveying the CS+ but also by the depression of sensory inputs unpaired to noxious stimuli.