运动诱导的前边缘皮层PV网络可塑性调节雄性小鼠恐惧记忆的表达。

IF 5.8 1区 医学 Q1 PSYCHIATRY
Neng-Yuan Hu, Xin Heng, Hao Li, Lang Huang, Yuan-Yue Dou, Yi-Hua Chen
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引用次数: 0

摘要

许多精神疾病,如焦虑症,其特征是对恐惧相关信息的异常处理。前边缘皮层(PL)的小白蛋白(PV)神经元在恐惧表达中起重要作用。然而,局部PV神经元网络的可塑性在远程恐惧记忆调控中的作用尚不清楚。在本研究中,我们发现近程和远程恐惧记忆的提取都诱导了前皮层的高PV可塑性。前皮层PV神经元的急性化学发生抑制降低了最近恐惧记忆的提取,抑制了恐惧诱导的向高PV神经元的转移,而这些效应在化学发生抑制三周后未被观察到。另一方面,这些神经元的慢性抑制导致恐惧记忆检索的持续减少和恐惧诱导的高pv可塑性的持续抑制。值得注意的是,自愿跑步模拟了PV神经元的慢性抑制作用,降低了恐惧记忆的表达,这可能是由PV神经元的化学发生激活所阻断的。总之,这些发现表明PV网络可塑性在PL中调节恐惧记忆表达的重要作用,并为某些焦虑障碍的治疗提供了替代方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Exercise-induced PV network plasticity in the prelimbic cortex regulates the expression of fear memory in male mice.

Many psychiatric disorders, such as anxiety disorders, are characterized by abnormal processing of fear-related information. Parvalbumin (PV) neurons in the prelimbic cortex (PL) are critically involved in fear expression. However, the role of plasticity of the local PV neuron network in the regulation of remote fear memory remains unknown. In this study, we showed that the retrieval of both recent and remote fear memory induced the high-PV plasticity in the PL. Acute chemogenetic inhibition of PV neurons in the PL decreased recent fear memory retrieval and suppressed the fear-induced shift toward high-PV neurons, while these effects were not observed three weeks after chemogenetic inhibition. On the other hand, chronic inhibition of these neurons led to a sustained reduction in fear memory retrieval and persistent suppression of fear-induced high-PV plasticity. Notably, voluntary running mimicked the effects of chronic inhibition of PV neurons and decreased the expression of fear memory, which could be blocked by chemogenetic activation of PV neurons. Together, these findings indicate an essential role for PV network plasticity in the PL in regulating fear memory expression and provide alternative methods for the treatment of certain anxiety disorders.

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来源期刊
CiteScore
11.50
自引率
2.90%
发文量
484
审稿时长
23 weeks
期刊介绍: Psychiatry has suffered tremendously by the limited translational pipeline. Nobel laureate Julius Axelrod''s discovery in 1961 of monoamine reuptake by pre-synaptic neurons still forms the basis of contemporary antidepressant treatment. There is a grievous gap between the explosion of knowledge in neuroscience and conceptually novel treatments for our patients. Translational Psychiatry bridges this gap by fostering and highlighting the pathway from discovery to clinical applications, healthcare and global health. We view translation broadly as the full spectrum of work that marks the pathway from discovery to global health, inclusive. The steps of translation that are within the scope of Translational Psychiatry include (i) fundamental discovery, (ii) bench to bedside, (iii) bedside to clinical applications (clinical trials), (iv) translation to policy and health care guidelines, (v) assessment of health policy and usage, and (vi) global health. All areas of medical research, including — but not restricted to — molecular biology, genetics, pharmacology, imaging and epidemiology are welcome as they contribute to enhance the field of translational psychiatry.
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