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Vibration-reduced anxiety-like behavior relies on ameliorating abnormalities of the somatosensory cortex and medial prefrontal cortex

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Neural Regeneration Research 2024年第6期19卷 1351-1359页

作者： Afzal Misrani Sidra Tabassum Tintin Wang Huixian Huang Jinxiang Jiang Hongjun Diao Yanping Zhao Zhen Huang Shaohua Tan Cheng Long Li Yang South China Normal University-Panyu Central Hospital Joint Laboratory of Translational Medical Research Panyu Central Hospital School of Life Sciences Guangzhou University School of Life Sciences South China Normal University Guangzhou Hongai Cultural Development Inc. 5. Yinguo Health Management Team College of Biophotonics South China Normal University

Tibetan singing bowls emit low-frequency sounds and produce perceptible harmonic tones and vibrations through manual tapping. The sounds the singing bowls produce have been shown to enhance relaxation and reduce anxiety. However, the underlying mechanism remains unclear. In this study, we used chronic restraint stress or sleep deprivation to establish mouse models of anxiety that exhibit anxiety-like behaviors. We then supplied treatment with singing bowls in a bottomless cage placed on the top of a cushion. We found that unlike in humans, the combination of harmonic tones and vibrations did not improve anxietylike behaviors in mice, while individual vibration components did. Additionally, the vibration of singing bowls increased the level of N-methyl-D-aspartate receptor 1 in the somatosensory cortex and prefrontal cortex of the mice, decreased the level of γ-aminobutyric acid A(GABA) receptor α 1 subtype, reduced the level of CaMKII in the prefrontal cortex, and increased the number of GABAergic interneurons. At the same time, electrophysiological tests showed that the vibration of singing bowls significantly reduced the abnormal low-frequency gamma oscillation peak frequency in the medial prefrontal cortex caused by stress restraint pressure and sleep deprivation. Results from this study indicate that the vibration of singing bowls can alleviate anxiety-like behaviors by reducing abnormal molecular and electrophysiological events in somatosensory and medial prefrontal cortex.

关键词： anxiety medial prefrontal cortex parvalbumin interneuron pressure somatosensory cortex Tibetan singing bowl vibration

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Distinct neuronal excitability alterations of medial prefrontal cortex in early-life neglect model of rats

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Animal Models and Experimental Medicine 2022年第3期5卷 274-280页

作者： Yu Zhang Xiuping Sun Changsong Dou Xianglei Li Ling Zhang Chuan Qin NHC Key Laboratory of Human Disease Comparative Medicine Institute of Laboratory Animal SciencesChinese Academy of Medical Sciences(CAMS)Comparative Medicine CenterPeking Union Medical College(PUMC)BeijingChina National Human Diseases Animal Model Resource Center BeijingChina Beijing Engineering Research Center for Experimental Animal Models of Human Critical Diseases BeijingChina International Center for Technology and Innovation of animal model BeijingChina Changping National laboratory(CPNL) BeijingChina

Object:Early-life neglect has irreversible emotional effects on the central nervous system.In this work,we aimed to elucidate distinct functional neural changes in me-dial prefrontal cortex(mPFC)of model rats.Methods:Maternal separation with early weaning was used as a rat model of early-life neglect.The excitation of glutamatergic and GABAergic neurons in rat mPFC was recorded and analyzed by whole-cell patch clamp.Results:Glutamatergic and GABAergic neurons of mPFC were distinguished by typi-cal electrophysiological properties.The excitation of mPFC glutamatergic neurons was significantly increased in male groups,while the excitation of mPFC GABAergic neurons was significant in both female and male groups,but mainly in terms of rest membrane potential and amplitude,respectively.Conclusions:Glutamatergic and GABAergic neurons in medial prefrontal cortex showed different excitability changes in a rat model of early-life neglect,which can contribute to distinct mechanisms for emotional and cognitive manifestations.

关键词： early-life neglect model GABAergic glutamatergic maternal separation with early weaning medial prefrontal cortex neuronal excitability

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Neurochemical metabolites in the medial prefrontal cortex in bipolar disorder A proton magnetic resonance spectroscopy study

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Neural Regeneration Research 2012年第36期7卷 2929-2936页

作者： Osman zdel Demet Kalayci Gülfizar Szeri-Varma Yilmaz Kiroglu Selim Tümkaya Tuge Toker-Ugurlu Department of Psychiatry Faculty of MedicinePamukkale University Department of Psychiatry Antalya Training and Research Hospital Department of Radiology Faculty of MedicinePamukkale University

The aim of this study was to investigate proton magnetic resonance spectroscopy metabolite values in the medial prefrontal cortex of individuals with euthymic bipolar disorder. The subjects consisted of 15 patients with euthymic bipolar disorder type I and 15 healthy controls. We performed proton magnetic resonance spectroscopy of the bilateral medial prefrontal cortex and measured levels of N-acetyl aspartate, choline and creatine. Levels of these three metabolites in the medial prefrontal cortex were found to be lower in patients with bipolar disorder compared with healthy controls. A positive correlation was found between illness duration and choline levels in the right medial prefrontal cortex. Our study suggests that during the euthymic period, there are abnormalities in cellular energy and membrane phospholipid metabolism in the medial prefrontal cortex, and that this may impair neuronal activity and integrity.

关键词： bipolar disorder proton magnetic resonance spectroscopy medial prefrontal cortex N-asetylaspartate choline creatine degradation mood disorder neurochemical metabolite illness duration neural regeneration

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Anticipatory activity in rat medial prefrontal cortex during a working memory task

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Neuroscience Bulletin 2012年第6期28卷 693-703页

作者： Wenwen Bai Tiaotiao Liu Hu Yi Shuangyan Li Xin Tian School of Biomedical Engineering Tianjin Medical University Laboratory of Neuroengineering Research Center of Basic MedicineTianjin Medical University

Objective Working memory is a key cognitive function in which the prefrontal cortex plays a crucial role. This study aimed to show the firing patterns of a neuronal population in the prefrontal cortex of the rat in a working memory task and to explore how a neuronal ensemble encodes a working memory event. Methods Sprague-Dawley rats were trained in a Y-maze until they reached an 80% correct rate in a working memory task. Then a 16-channel microelectrode array was implanted in the prefrontal cortex. After recovery, neuronal population activity was recorded during the task, using the Cerebus data-acquisition system. Spatio-temporal trains of action potentials were obtained from the original neuronal population signals. Results During the Y-maze working memory task, some neurons showed significantly in- creased firing rates and evident neuronal ensemble activity. Moreover, the anticipatory activity was associated with the delayed alternate choice of the upcoming movement. In correct trials, the averaged pre-event firing rate （10.86 ± 1.82 spikes/ bin） was higher than the post-event rate （8.17 ± 1.15 spikes/bin）（P 〈0.05）. However, in incorrect trials, the rates did not differ. Conclusion The results indicate that the anticipatory activity of a neuronal ensemble in the prefrontal cortex may play a role in encoding working memory events.

关键词： anticipatory activity working memory rat medial prefrontal cortex neuronal ensemble

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Effects of Melatonin Levels on Neurotoxicity of the medial prefrontal cortex in a Rat Model of Parkinson＇s Disease

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Chinese Medical Journal 2017年第22期130卷 2726-2731页

作者： Yan Li Shu-Mei Wang Lei Guo Jian Zhu Ying Wang Lei Li Yan-Xin Zhao Department of Neurology Jinan Central Hospital Affiliated to Shandong University Jinan Shandong 250013 China General Medical Teaching and Research Section Jinan Central Hospital Affiliated to Shandong University Jinan Shandong 250013 China Department of Medical Imaging Jinan Central Hospital Affiliated to Shandong University Jinan Shandong 250013 China Department of Medical Imaging Shandong Provincial Hospital Jinan Shandong 250014 China

Background： Damage of the medial prefrontal cortex （mPFC） results in similar characteristics to the cognitive deficiency seen with the progress of Parkinson＇s disease （PD）. Since the course of mPFC damage is still unclear, our study aimed to investigate the effects of melatonin （MT） on neurotoxicity in the mPFC of a rat model of PD. Methods： One hundred and fifty-four normal, male Wistar rats were randomly divided into the following five groups： normal ＋ normal saline （NS）, normal ＋ 6-hydroxydopamine （6-OHDA）, sham pinealectomy （PX）＋ 6-OHDA, PX ＋ 6-OHDA, and MT ＋ 6-OHDA. 6-OHDA was injected into the right substantia nigra pars compacta （SNc） and ventral tegmental area （VTA） of each group, except normal ＋ NS, 60 days after the PX. In the MT treatment group, MT was administered immediately after the intraperitoneal injection at 4 p.m. every day, for 14 days. Neuronal apoptosis in the mPFC was exalnined using the TUNEL method, while the expression oftyrosine hydroxylase （TH）, Bax, and Bcl-2 in this region was measured using immunohistochemistry. The concentration of malondialdehyde （MDA） in the mPFC was examined using the thioharbituric acid method. Results： Rats in the normal ＋ 6-OHDA and sham PX ＋ 6-OHDA groups were combined into one group （Group N ＋ 6-OHDA） since there was no significant discrepancy between the groups for all the detected parameters. Apoptosis of cells in the NS, MT ＋ 6-OHDA, N ＋ 6-OH DA, and PX ＋ 6-OHDA groups was successively significantly increased （Hc = 256.25, P 〈 0.001 ）. The gray value of TH （＋） fibers in the NS, MT ＋ 6-OHDA, N ＋ 6-OHDA, and PX ＋ 6-OHDA groups was also successively significantly increased （F= 99.33, P 〈 0.001 ）. The staining intensities of Bax and Bcl-2 were as follows： Group NS ＋/＋, Group MT ＋ 6-OHDA ＋＋/＋, Group N ＋ 6-OHDA ＋＋/＋, and PX ＋ 6-OHDA ＋＋＋/＋. The concentrations of MDA in the NS, MT ＋ 6-OHDA, N ＋ 6-OHDA, and PX ＋ 6-OHDA groups were significantly increased in sequence （Hc = 296.309, P 〈 0.001 ）. Conclusions： Neuronal damage of the VTA by 6-OHDA might induce VTA-mP

关键词： medial prefrontal cortex Melatonin Pinealectomy Tyrosine Hydroxylase Ventral Tegmental Area

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Reversal of Social Recognition Deficit in Adult Mice with MECP2 Duplication via Normalization of MeCP2 in the medial prefrontal cortex

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Neuroscience Bulletin 2020年第6期36卷 570-584页

作者： Bin Yu Bo Yuan Jian-Kun Dai Tian-lin Cheng Sheng-Nan Xia Ling-Jie He Yi-Ting Yuan Yue-Fang Zhang Hua-Tai Xu Fu-Qiang Xu Zhi-Feng Liang Zi-Long Qiu Institute of Neuroscience State Key Laboratory of NeuroscienceChinese Academy of Sciences Center for Excellence in Brain Science and Intelligence TechnologyChinese Academy of SciencesShanghai 200031China University of Chinese Academy of Sciences Beijing 100049China Department of Molecular and Human Genetics Howard Hughes Medical InstituteBaylor College of MedicineHoustonTX 77030USA Wuhan Institute of Physics and Mathematics Chinese Academy of SciencesWuhan 430071China

Methyl-CpG binding protein 2(MeCP2) is a basic nuclear protein involved in the regulation of gene expression and microRNA processing.Duplication of MECP2-containing genomic segments causes MECP2 duplication syndrome,a severe neurodevelopmental disorder characterized by intellectual disability,motor dysfunction,heightened anxiety,epilepsy,autistic phenotypes,and early death.Reversal of the abnormal phenotypes in adult mice with MECP2 duplication(MECP2-TG) by normalizing the MeCP2 levels across the whole brain has been demonstrated.However,whether different brain areas or neural circuits contribute to different aspects of the behavioral deficits is still unknown.Here,we found that MECP2-TG mice showed a significant social recognition deficit,and were prone to display aversive-like behaviors,including heightened anxiety-like behaviors and a fear generalization phenotype.In addition,reduced locomotor activity was observed in MECP2-TG mice.However,appetitive behaviors and learning and memory were comparable in MECP2-TG and wild-type mice.Functional magnetic resonance imaging illustrated that the differences between MECP2-TG and wild-type mice were mainly concentrated in brain areas regulating emotion and social behaviors.We used the CRISPR-Cas9 method to restore normal MeCP2 levels in the medial prefrontal cortex(mPFC) and bed nuclei of the stria terminalis(BST) of adult MECP2-TG mice,and found that normalization of MeCP2 levels in the mPFC but not in the BST reversed the social recognition deficit.These data indicate that the mPFC is responsible for the social recognition deficit in the transgenic mice,and provide new insight into potential therapies for MECP2 duplication syndrome.

关键词： MECP2 duplication medial prefrontal cortex Social recognition deficit CRISPR-Cas9

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Role of 5-hydroxytryptamine type 3 receptors in the regulation of anxiety reactions

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2024年第1期25卷 23-37页

作者： Yinan DU Zhiwei LI Yukui ZHAO Jing HAN Weiping HU Zhiqiang LIU MOE Key Laboratory of Modern Teaching Technology Shaanxi Normal UniversityXi’an710062China

5-Hydroxytryptamine(5-HT)type 3 receptor(5-HT_(3)R)is the only type of ligand-gated ion channel in the 5-HT receptor family.Through the high permeability of Na+,K+,and Ca2+and activation of subsequent voltage-gated calcium channels(VGCCs),5-HT_(3)R induces a rapid increase of neuronal excitability or the release of neurotransmitters from axon terminals in the central nervous system(CNS).5-HT_(3)Rs are widely expressed in the medial prefrontal cortex(mPFC),amygdala(AMYG),hippocampus(HIP),periaqueductal gray(PAG),and other brain regions closely associated with anxiety reactions.They have a bidirectional regulatory effect on anxiety reactions by acting on different types of cells in different brain regions.5-HT_(3)Rs mediate the activation of the cholecystokinin(CCK)system in the AMYG,and theγ-aminobutyric acid(GABA)“disinhibition”mechanism in the prelimbic area of the mPFC promotes anxiety by the activation of GABAergic intermediate inhibitory neurons(IINs).In contrast,a 5-HT_(3)R-induced GABA“disinhibition”mechanism in the infralimbic area of the mPFC and the ventral HIP produces anxiolytic effects.5-HT_(2)R-mediated regulation of anxiety reactions are also activated by 5-HT_(3)R-activated 5-HT release in the HIP and PAG.This provides a theoretical basis for the treatment of anxiety disorders or the production of anxiolytic drugs by targeting 5-HT_(3)Rs.However,given the circuit specific modulation of 5-HT_(3)Rs on emotion,systemic use of 5-HT_(3)R agonism or antagonism alone seems unlikely to remedy anxiety,which deeply hinders the current clinical application of 5-HT_(3)R drugs.Therefore,the exploitation of circuit targeting methods or a combined drug strategy might be a useful developmental approach in the future.

关键词： 5-Hydroxytryptamine type 3 receptor(5-HT_(3)R) Anxiety medial prefrontal cortex Amygdala Hippocampus Periaqueductal gray

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In vivo imaging reveals a synchronized correlation among neurotransmitter dynamics during propofol and sevoflurane anesthesia

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Zoological Research 2024年第3期45卷 679-690页

作者： Gao-Lin Qiu Li-Jun Peng Peng Wang Zhi-Lai Yang Ji-Qian Zhang Hu Liu Xiao-Na Zhu Jin Rao Xue-Sheng Liu Department of Anesthesiology First Affiliated Hospital of Anhui Medical UniversityHefeiAnhui 230022China School of Life Science and Technology ShanghaiTech UniversityShanghai 201210China

General anesthesia is widely applied in clinical practice.However,the precise mechanism of loss of consciousness induced by general anesthetics remains unknown.Here,we measured the dynamics of five neurotransmitters,includingγ-aminobutyric acid,glutamate,norepinephrine,acetylcholine,and dopamine,in the medial prefrontal cortex and primary visual cortex of C57BL/6 mice through in vivo fiber photometry and genetically encoded neurotransmitter sensors under anesthesia to reveal the mechanism of general anesthesia from a neurotransmitter perspective.Results revealed that the concentrations of γ-aminobutyric acid,glutamate,norepinephrine,and acetylcholine increased in the cortex during propofol-induced loss of consciousness.Dopamine levels did not change following the hypnotic dose of propofol but increased significantly following surgical doses of propofol anesthesia.Notably,the concentrations of the five neurotransmitters generally decreased during sevoflurane-induced loss of consciousness.Furthermore,the neurotransmitter dynamic networks were not synchronized in the non-anesthesia groups but were highly synchronized in the anesthetic groups.These findings suggest that neurotransmitter dynamic network synchronization may cause anesthetic-induced loss of consciousness.

关键词： General anesthesia Loss of consciousness In vivo neurotransmitter imaging medial prefrontal cortex Primary visual cortex

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Brain region-specific roles of brain-derived neurotrophic factor in social stress-induced depressive-like behavior

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Neural Regeneration Research 2025年第1期20卷 159-173页

作者： Man Han Deyang Zeng Wei Tan Xingxing Chen Shuyuan Bai Qiong Wu Yushan Chen Zhen Wei Yufei Mei Yan Zeng Brain Science and Advanced Technology Institute Wuhan University of Science and TechnologyWuhanHubei ProvinceChina Geriatric Hospital Affiliated to Wuhan University of Science and Technology WuhanHubei ProvinceChina School of Public Health Wuhan University of Science and TechnologyWuhanHubei ProvinceChina

Brain-derived neurotrophic factor is a key factor in stress adaptation and avoidance of a social stress behavioral response.Recent studies have shown that brain-derived neurotrophic factor expression in stressed mice is brain region–specific,particularly involving the corticolimbic system,including the ventral tegmental area,nucleus accumbens,prefrontal cortex,amygdala,and hippocampus.Determining how brain-derived neurotrophic factor participates in stress processing in different brain regions will deepen our understanding of social stress psychopathology.In this review,we discuss the expression and regulation of brain-derived neurotrophic factor in stress-sensitive brain regions closely related to the pathophysiology of depression.We focused on associated molecular pathways and neural circuits,with special attention to the brain-derived neurotrophic factor–tropomyosin receptor kinase B signaling pathway and the ventral tegmental area–nucleus accumbens dopamine circuit.We determined that stress-induced alterations in brain-derived neurotrophic factor levels are likely related to the nature,severity,and duration of stress,especially in the above-mentioned brain regions of the corticolimbic system.Therefore,BDNF might be a biological indicator regulating stress-related processes in various brain regions.

关键词： amygdala chronic mild stress chronic social defeat stress corticolimbic system depression hippocampus medial prefrontal cortex nucleus accumbens social stress models ventral tegmental area

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Lesions of medial prefrontal cortex prevent stress but not prime induced reinstatement of morphine conditioned place preference

Lesions of medial prefrontal cortex prevent stress but not p...

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第三届中日双边药理学和临床药理学学术会议

作者： HAO Yue YANG Jing-Yu WU Chun-Fu (Department of Pharmacology,Shenyang Pharmaceutical University,Shenyang 110016,China)

AIM Considerable evidence has implicated the medial prefrontal cortex (mPFC) in morphine addic- tion especially in the process of relapse.In order to further investigate the role of the mPFC in stress and drug priming induced relapse,the present study examined the effects of the mPFC lesions on footshock stress and morphine prim- ing induced reinstatement of conditioned place preference (CPP).METHODS Mice were trained with morphine (10 mg·kg,ip) or saline for 6 d.After the place pref- erence was established,each mouse received sham or bi- lateral kainic acid lesions in the mPFC and allowed to re- cover from the surgery for 9 d,then a priming injection of morphine (2 mg·kg,ip) or a 20 min foot shock stress (0.2 mA,a width of 0.5 s,the off time distributed ran- domly between 10 and 70 s with an average of 40 s) was given to reinstate the extinguished CPP.RESULTS The post-conditioning lesions of the mPFC prevented foot shock but not drug priming induced reinstatement of CPP.CON- CLUSION These results provide the first direct evidence that the mPFC may be involved in the stress,but not drug priming induced reinstatement of CPP and also suggest that different neural subtracts be involved in stress and drug priming induced reinstatement of morphine CPP.

关键词： medial prefrontal cortex morphine conditioned place preference footshock stress drug priming

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