Tac2、NkB 和 Nk3 受体在正常和失调的恐惧记忆巩固中的作用。
A role for Tac2, NkB, and Nk3 receptor in normal and dysregulated fear memory consolidation.
机构信息
Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GA 30329, USA; Center for Behavioral Neuroscience, Yerkes National Primate Research Center, Atlanta, GA 30329, USA.
Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GA 30329, USA; Center for Behavioral Neuroscience, Yerkes National Primate Research Center, Atlanta, GA 30329, USA.
出版信息
Neuron. 2014 Jul 16;83(2):444-454. doi: 10.1016/j.neuron.2014.05.028. Epub 2014 Jun 26.
The centromedial amygdala (CeM), a subdivision of the central amygdala (CeA), is believed to be the main output station of the amygdala for fear expression. We provide evidence that the Tac2 gene, expressed by neurons specifically within the CeM, is required for modulating fear memories. Tac2 is colocalized with GAD65 and CaMKIIα but not with PKCd and Enk neurons in the CeM. Moreover, the Tac2 product, NkB, and its specific receptor, Nk3R, are also involved in the consolidation of fear memories. Increased Tac2 expression, through a stress-induced PTSD-like model, or following lentiviral CeA overexpression, are sufficient to enhance fear consolidation. This effect is blocked by the Nk3R antagonist osanetant. Concordantly, silencing of Tac2-expressing neurons in CeA with DREADDs impairs fear consolidation. Together, these studies further our understanding of the role of the Tac2 gene and CeM in fear processing and may provide approaches to intervention for fear-related disorders.
中央杏仁核的中央内侧核（CeM）被认为是杏仁核中恐惧表达的主要输出站。我们提供的证据表明，Tac2 基因在 CeM 内特定的神经元中表达，对于调节恐惧记忆是必需的。Tac2 与 GAD65 和 CaMKIIα 共定位，但与 CeM 中的 PKCd 和 Enk 神经元不同。此外，Tac2 产物 NkB 及其特定受体 Nk3R 也参与了恐惧记忆的巩固。通过应激诱导的 PTSD 样模型或通过慢病毒 CeA 过表达增加 Tac2 表达足以增强恐惧的巩固。这种效应被 Nk3R 拮抗剂 osanetant 阻断。一致地，使用 DREADDs 沉默 CeA 中表达 Tac2 的神经元会损害恐惧的巩固。总之，这些研究进一步了解了 Tac2 基因和 CeM 在恐惧处理中的作用，并可能为恐惧相关障碍的干预提供方法。
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