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肿瘤坏死因子-α调控梨状前皮质中兴奋性和抑制性突触的经验依赖性可塑性。

TNF-α Orchestrates Experience-Dependent Plasticity of Excitatory and Inhibitory Synapses in the Anterior Piriform Cortex.

作者信息

Guo Anni, Lau Chunyue Geoffrey

机构信息

Department of Neuroscience, City University of Hong Kong, Kowloon, Hong Kong SAR, China.

Shenzhen Research Institute, City University of Hong Kong, Shenzhen, China.

出版信息

Front Neurosci. 2022 Apr 26;16:824454. doi: 10.3389/fnins.2022.824454. eCollection 2022.

DOI:10.3389/fnins.2022.824454
PMID:35557610
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9086849/
Abstract

Homeostatic synaptic plasticity, which induces compensatory modulation of synapses, plays a critical role in maintaining neuronal circuit function in response to changing activity patterns. Activity in the anterior piriform cortex (APC) is largely driven by ipsilateral neural activity from the olfactory bulb and is a suitable system for examining the effects of sensory experience on cortical circuits. Pro-inflammatory cytokine tumor necrosis factor-α (TNF-α) can modulate excitatory and inhibitory synapses, but its role in APC is unexplored. Here we examined the role of TNF-α in adjusting synapses in the mouse APC after experience deprivation via unilateral naris occlusion. Immunofluorescent staining revealed that activity deprivation increased excitatory, and decreased inhibitory, synaptic density in wild-type mice, consistent with homeostatic regulation. Quantitative RT-PCR showed that naris occlusion increased the expression of Tnf mRNA in APC. Critically, occlusion-induced plasticity of excitatory and inhibitory synapses was completely blocked in the Tnf knockout mouse. Together, these results show that TNF-α is an important orchestrator of experience-dependent plasticity in the APC.

摘要

稳态突触可塑性可诱导突触的代偿性调节,在响应不断变化的活动模式时,对维持神经元回路功能起着关键作用。前梨状皮质(APC)的活动很大程度上由来自嗅球的同侧神经活动驱动,是研究感觉经验对皮质回路影响的合适系统。促炎细胞因子肿瘤坏死因子-α(TNF-α)可调节兴奋性和抑制性突触,但其在APC中的作用尚未得到探索。在此,我们通过单侧鼻孔闭塞剥夺经验后,研究了TNF-α在调节小鼠APC突触中的作用。免疫荧光染色显示,活动剥夺增加了野生型小鼠的兴奋性突触密度,降低了抑制性突触密度,这与稳态调节一致。定量逆转录聚合酶链反应表明,鼻孔闭塞增加了APC中Tnf mRNA的表达。至关重要的是,在Tnf基因敲除小鼠中,闭塞诱导的兴奋性和抑制性突触可塑性被完全阻断。这些结果共同表明,TNF-α是APC中经验依赖性可塑性的重要协调因子。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ed5/9086849/a0f876c94abf/fnins-16-824454-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ed5/9086849/47f6a9510c24/fnins-16-824454-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ed5/9086849/837160169d29/fnins-16-824454-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ed5/9086849/f131dc8bf4cf/fnins-16-824454-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ed5/9086849/e47bcb30ed0b/fnins-16-824454-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ed5/9086849/a0f876c94abf/fnins-16-824454-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ed5/9086849/47f6a9510c24/fnins-16-824454-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ed5/9086849/837160169d29/fnins-16-824454-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ed5/9086849/f131dc8bf4cf/fnins-16-824454-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ed5/9086849/e47bcb30ed0b/fnins-16-824454-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ed5/9086849/a0f876c94abf/fnins-16-824454-g005.jpg

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