杏仁核中枢有助于小脑学习过程中的刺激促进和刺激前警觉

IF 2.2 4区 心理学 Q3 BEHAVIORAL SCIENCES
Sean J. Farley, John H. Freeman
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引用次数: 0

摘要

我们之前的研究发现,中央杏仁核(CeA)会利用麝香草酚失活调节小脑依赖性眼动条件反射(EBC)。我们还发现,从训练一开始,CeA 失活就会降低条件刺激(CS)期间的小脑神经元活动。基于这些发现,我们假设CeA促进了CS对小脑的输入。目前的研究使用光遗传学方法,在雄性大鼠的EBC过程中用弓形视紫红质(Arch)对CeA进行抑制,用通道视紫红质(ChR2)对CeA进行兴奋,从而验证了CS促进假说。光遗传操作在400毫秒音调CS期间或400毫秒音调CS前期间进行。正如 CS 促进假说所预测的那样,CS 期间的 CeA 抑制会损害 EBC,而 CS 期间的 CeA 兴奋会促进 EBC。意想不到的是,CS 前的 CeA 抑制也会损害 EBC,而 CS 前通路中的 CeA 兴奋则不会促进 EBC。这些结果表明,CeA 在 CS 前阶段有助于 CS 促进和警觉。CeA的这些假定功能可能是通过从CeA到小脑的不同输出途径介导的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Central amygdala contributes to stimulus facilitation and pre-stimulus vigilance during cerebellar learning

Our previous studies found that the central amygdala (CeA) modulates cerebellum-dependent eyeblink conditioning (EBC) using muscimol inactivation. We also found that CeA inactivation decreases cerebellar neuronal activity during the conditional stimulus (CS) from the start of training. Based on these findings, we hypothesized that the CeA facilitates CS input to the cerebellum. The current study tested the CS facilitation hypothesis using optogenetic inhibition with archaerhodopsin (Arch) and excitation with channelrhodopsin (ChR2) of the CeA during EBC in male rats. Optogenetic manipulations were administered during the 400 ms tone CS or during a 400 ms pre-CS period. As predicted by the CS facilitation hypothesis CeA inhibition during the CS impaired EBC and CeA excitation during the CS facilitated EBC. Unexpectedly, CeA inhibition just prior to the CS also impaired EBC, while CeA excitation during the pre-CS pathway did not facilitate EBC. The results suggest that the CeA contributes to CS facilitation and vigilance during the pre-CS period. These putative functions of the CeA may be mediated through separate output pathways from the CeA to the cerebellum.

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来源期刊
CiteScore
5.10
自引率
7.40%
发文量
77
审稿时长
12.6 weeks
期刊介绍: Neurobiology of Learning and Memory publishes articles examining the neurobiological mechanisms underlying learning and memory at all levels of analysis ranging from molecular biology to synaptic and neural plasticity and behavior. We are especially interested in manuscripts that examine the neural circuits and molecular mechanisms underlying learning, memory and plasticity in both experimental animals and human subjects.
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