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前额叶和海马θ节律在导水管周围灰质诱发的“恐慌”期间表现出类似抗焦虑的变化。

Prefrontal and hippocampal theta rhythm show anxiolytic-like changes during periaqueductal-elicited "panic" in rats.

机构信息

Department of Psychology and Brain Health Research Centre, University of Otago, Dunedin, New Zealand.

出版信息

Hippocampus. 2022 Sep;32(9):679-694. doi: 10.1002/hipo.23459. Epub 2022 Aug 2.

DOI:10.1002/hipo.23459
PMID:35916172
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9540356/
Abstract

Anxiety and panic are both elicited by threat and co-occur clinically. But, at the neural level, anxiety appears to inhibit the generation of panic; and vice versa. Anxiety and panic are thought to engage more anterior (a) and mid-posterior (m) parts of the periaqueductal gray (PAG), respectively. Anxiety also engages the hippocampus and medial prefrontal cortex. Here, we tested if mPAG but not aPAG stimulation would suppress prefrontal and hippocampal theta rhythm as do anxiolytic drugs. Twelve male rats with implanted electrodes were stimulated alternately (30 s interval) in the left PAG or right reticular formation (reticularis pontis oralis [RPO]-as a positive control) with recording in the left prelimbic cortex and left and right hippocampus. PAG stimulation was set to produce freezing and RPO to produce 7-8 Hz theta rhythm before tests lasting 10 min on each of 5 days. mPAG stimulation decreased, and aPAG increased, theta power at all sites during elicited freezing. mPAG, but not aPAG, stimulation decreased prefrontal theta frequency. Stimulation did not substantially change circuit dynamics (pairwise phase consistency and partial directed coherence). Together with previous reports, our data suggest that panic- and anxiety-control systems are mutually inhibitory, and neural separation of anxiety and panic extends down to the aPAG and mPAG, respectively. Our findings are consistent with recent proposals that fear and anxiety are controlled by parallel neural hierarchies extending from PAG to the prefrontal cortex.

摘要

焦虑和恐慌都是由威胁引起的,临床上常同时发生。但是,在神经水平上,焦虑似乎抑制了恐慌的产生;反之亦然。焦虑和恐慌被认为分别涉及到中脑导水管周围灰质(periaqueductal gray,PAG)的前(a)和中后(m)部分。焦虑还涉及海马体和内侧前额叶皮层。在这里,我们测试了中脑导水管周围灰质(periaqueductal gray,PAG)刺激是否会像抗焦虑药物一样抑制前额叶和海马体的θ节律,而不是前脑导水管周围灰质(periaqueductal gray,PAG)刺激。12 只植入电极的雄性大鼠在左侧 PAG 或右侧网状结构(reticularis pontis oralis [RPO] - 作为阳性对照)交替刺激(30 秒间隔),在左侧前额叶皮层和左侧和右侧海马体记录。PAG 刺激设置为产生冻结,RPO 刺激在每次 5 天的 10 分钟测试前产生 7-8 Hz 的θ节律。PAG 刺激减少,aPAG 增加,在诱发的冻结期间,所有部位的θ功率增加。mPAG 刺激降低,aPAG 刺激增加前额叶θ频率。刺激并没有实质性地改变电路动力学(成对相位一致性和部分定向相干性)。结合以前的报告,我们的数据表明,恐慌和焦虑控制系统是相互抑制的,焦虑和恐慌的神经分离分别延伸到 aPAG 和 mPAG。我们的发现与最近的提议一致,即恐惧和焦虑是由平行的神经层次结构控制的,从 PAG 延伸到前额叶皮层。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b5c9/9540356/662b79fb0f6d/HIPO-32-679-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b5c9/9540356/c6ceda85e809/HIPO-32-679-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b5c9/9540356/4f97e005af05/HIPO-32-679-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b5c9/9540356/8ef1823dc998/HIPO-32-679-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b5c9/9540356/9ae0a6500613/HIPO-32-679-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b5c9/9540356/ee00f6ffc9bc/HIPO-32-679-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b5c9/9540356/97fd024dc53b/HIPO-32-679-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b5c9/9540356/662b79fb0f6d/HIPO-32-679-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b5c9/9540356/c6ceda85e809/HIPO-32-679-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b5c9/9540356/4f97e005af05/HIPO-32-679-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b5c9/9540356/8ef1823dc998/HIPO-32-679-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b5c9/9540356/9ae0a6500613/HIPO-32-679-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b5c9/9540356/ee00f6ffc9bc/HIPO-32-679-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b5c9/9540356/97fd024dc53b/HIPO-32-679-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b5c9/9540356/662b79fb0f6d/HIPO-32-679-g001.jpg

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