Translational Neuroscience最新文献_第10页

Comprehensive behavioral study of C57BL/6.KOR-ApoE^shl mice. C57BL/6的综合行为学研究KOR-ApoEshl老鼠。

IF 2.1 4区医学

Translational Neuroscience Pub Date : 2023-01-01 DOI: 10.1515/tnsci-2022-0284

Hiroshi Ueno, Yu Takahashi, Shinji Murakami, Kenta Wani, Tetsuji Miyazaki, Yosuke Matsumoto, Motoi Okamoto, Takeshi Ishihara

{"title":"Comprehensive behavioral study of C57BL/6.KOR-ApoEshl mice.","authors":"Hiroshi Ueno, Yu Takahashi, Shinji Murakami, Kenta Wani, Tetsuji Miyazaki, Yosuke Matsumoto, Motoi Okamoto, Takeshi Ishihara","doi":"10.1515/tnsci-2022-0284","DOIUrl":"https://doi.org/10.1515/tnsci-2022-0284","url":null,"abstract":"Background: Apolipoprotein E (ApoE) is associated with Alzheimer's disease (AD) and cognitive dysfunction in elderly individuals. There have been extensive studies on behavioral abnormalities in ApoE-deficient (Apoeshl) mice, which have been described as AD mouse models. Spontaneously hyperlipidemic mice were discovered in 1999 as ApoE-deficient mice due to ApoE gene mutations. However, behavioral abnormalities in commercially available Apoeshl mice remain unclear. Accordingly, we aimed to investigate the behavioral abnormalities of Apoeshl mice.Results: Apoeshl mice showed decreased motor skill learning and increased anxiety-like behavior toward heights. Apoeshl mice did not show abnormal behavior in the Y-maze test, open-field test, light/dark transition test, and passive avoidance test.Conclusion: Our findings suggest the utility of Apoeshl mice in investigating the function of ApoE in the central nervous system.","PeriodicalId":23227,"journal":{"name":"Translational Neuroscience","volume":"14 1","pages":"20220284"},"PeriodicalIF":2.1,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10314129/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9735968","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

miR-101-3p improves neuronal morphology and attenuates neuronal apoptosis in ischemic stroke in young mice by downregulating HDAC9. miR-101-3p通过下调hdac - 9，改善缺血性脑卒中幼鼠神经元形态，减轻神经元凋亡。

IF 2.1 4区医学

Translational Neuroscience Pub Date : 2023-01-01 DOI: 10.1515/tnsci-2022-0286

Mengru Zhang, Jianjun Wang, Jinfang Li, Fanxin Kong, Songjun Lin

{"title":"miR-101-3p improves neuronal morphology and attenuates neuronal apoptosis in ischemic stroke in young mice by downregulating HDAC9.","authors":"Mengru Zhang, Jianjun Wang, Jinfang Li, Fanxin Kong, Songjun Lin","doi":"10.1515/tnsci-2022-0286","DOIUrl":"https://doi.org/10.1515/tnsci-2022-0286","url":null,"abstract":"Objective: MiRNAs play a key role in ischemic stroke (IS). Although miR-101-3p can participate in multiple disease processes, its role and mechanism in IS are not clear. The aim of the present study was to observe the effect of miR-101-3p activation on IS in young mice and the role of HDAC9 in this effect.Methods: The young mice were first subjected to transient middle cerebral artery occlusion (tMCAO) or sham surgery, and the cerebral infarct area was assessed with 2,3,5-triphenyltetrazolium chloride staining. Meanwhile, the expressions of miR-101-3p and HDAC9 were tested using RT-qPCR or western blot. Besides, neuron morphology and apoptosis were confirmed using Nissl staining and TUNEL staining.Results: We first verified that miR-101-3p was downregulated and HDAC9 was upregulated in the brain tissue of tMCAO young mice. Moreover, we proved that overexpression of miR-101-3p could improve cerebral infarction, neuronal morphology, and neuronal apoptosis in tMCAO young mice by lowering the expression of HDAC9.Conclusions: Activation of miR-101-3p can protect against IS in young mice, and its mechanism is relevant to the inhibition of HDAC9. Therefore, miR-101-3p and HDAC9 might be the latent targets for IS therapy.","PeriodicalId":23227,"journal":{"name":"Translational Neuroscience","volume":"14 1","pages":"20220286"},"PeriodicalIF":2.1,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10224617/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9549462","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

An interventional study of baicalin on neuronal pentraxin-1, neuronal pentraxin-2, and C-reactive protein in Alzheimer's disease rat model. 黄芩苷对阿尔茨海默病大鼠模型神经元戊烷素-1、戊烷素-2及c反应蛋白的干预研究。

IF 2.1 4区医学

Translational Neuroscience Pub Date : 2023-01-01 DOI: 10.1515/tnsci-2022-0298

Jing-Kun Zhao, Si-Jia Hou, Ji-Wei Zhao, Hong-Li Yu, Shu-Rong Duan

{"title":"An interventional study of baicalin on neuronal pentraxin-1, neuronal pentraxin-2, and C-reactive protein in Alzheimer's disease rat model.","authors":"Jing-Kun Zhao, Si-Jia Hou, Ji-Wei Zhao, Hong-Li Yu, Shu-Rong Duan","doi":"10.1515/tnsci-2022-0298","DOIUrl":"https://doi.org/10.1515/tnsci-2022-0298","url":null,"abstract":"Background: Baicalin has been shown to promote spatial learning and neural regeneration, which might increase the differentiation of neural stem cells in Alzheimer's disease (AD) rat models. We aimed to study the role of baicalin on neuronal pentraxin-1 (NPTX-1), neuronal pentraxin-2 (NPTX-2), and C-reactive protein (CRP) in AD model rats.Methods: The 30 male Sprague Dawley rats were divided into three groups: the control group, the AD model group, and the AD + baicalin group. Then, the Morris water maze was used to verify the effect of baicalin on the memory and spatial learning of rats. Immunohistochemistry and immunofluorescence were used to observe the expression of NPTX-1, NPTX-2, and CRP in brain tissue.Results: Compared with the AD model group, the AD rats treated with baicalin spent significantly less time finding escape latencies (P = 0.008) and had longer cross-platform times in the target quadrant (P = 0.015). In addition, the AD + baicalin group had significantly higher numbers of hippocampal neurons compared with the AD model group (P < 0.05). Baicalin also obviously decreased the apoptosis of neurons. Moreover, compared with the AD model group, the NPTX-1 and CRP expression in the AD + baicalin group was significantly reduced (P = 0.000) while the expression of NPTX-2 in the brain tissue of AD rats was significantly increased (P = 0.000).Conclusions: Baicalin can play a therapeutic role by downregulating NPTX-1, upregulating NPTX-2, and downregulating CPR in AD model rats.","PeriodicalId":23227,"journal":{"name":"Translational Neuroscience","volume":"14 1","pages":"20220298"},"PeriodicalIF":2.1,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10500638/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10306731","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Nanotechnology-based drug delivery for the treatment of CNS disorders. 基于纳米技术的药物递送治疗中枢神经系统疾病。

IF 2.1 4区医学

Translational Neuroscience Pub Date : 2022-12-31 eCollection Date: 2022-01-01 DOI: 10.1515/tnsci-2022-0258

Khushi R Mittal, Nandini Pharasi, Bhavya Sarna, Manisha Singh, Rachana, Shazia Haider, Sachin Kumar Singh, Kamal Dua, Saurabh Kumar Jha, Abhijit Dey, Shreesh Ojha, Shalini Mani, Niraj Kumar Jha

{"title":"Nanotechnology-based drug delivery for the treatment of CNS disorders.","authors":"Khushi R Mittal, Nandini Pharasi, Bhavya Sarna, Manisha Singh, Rachana, Shazia Haider, Sachin Kumar Singh, Kamal Dua, Saurabh Kumar Jha, Abhijit Dey, Shreesh Ojha, Shalini Mani, Niraj Kumar Jha","doi":"10.1515/tnsci-2022-0258","DOIUrl":"10.1515/tnsci-2022-0258","url":null,"abstract":"Approximately 6.8 million people die annually because of problems related to the central nervous system (CNS), and out of them, approximately 1 million people are affected by neurodegenerative diseases that include Alzheimer's disease, multiple sclerosis, epilepsy, and Parkinson's disease. CNS problems are a primary concern because of the complexity of the brain. There are various drugs available to treat CNS disorders and overcome problems with toxicity, specificity, and delivery. Barriers like the blood-brain barrier (BBB) are a challenge, as they do not allow therapeutic drugs to cross and reach their target. Researchers have been searching for ways to allow drugs to pass through the BBB and reach the target sites. These problems highlight the need of nanotechnology to alter or manipulate various processes at the cellular level to achieve the desired attributes. Due to their nanosize, nanoparticles are able to pass through the BBB and are an effective alternative to drug administration and other approaches. Nanotechnology has the potential to improve treatment and diagnostic techniques for CNS disorders and facilitate effective drug transfer. With the aid of nanoengineering, drugs could be modified to perform functions like transference across the BBB, altering signaling pathways, targeting specific cells, effective gene transfer, and promoting regeneration and preservation of nerve cells. The involvement of a nanocarrier framework inside the delivery of several neurotherapeutic agents used in the treatment of neurological diseases is reviewed in this study.","PeriodicalId":23227,"journal":{"name":"Translational Neuroscience","volume":"13 1","pages":"527-546"},"PeriodicalIF":2.1,"publicationDate":"2022-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9883694/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10661258","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 8

Correlations between EEG and intestinal electrical stimulation. 脑电图与肠道电刺激之间的相关性。

IF 1.8 4区医学

Translational Neuroscience Pub Date : 2022-12-06 eCollection Date: 2022-01-01 DOI: 10.1515/tnsci-2022-0256

Nora Vanessa de Camp, Jürgen Bergeler

{"title":"Correlations between EEG and intestinal electrical stimulation.","authors":"Nora Vanessa de Camp, Jürgen Bergeler","doi":"10.1515/tnsci-2022-0256","DOIUrl":"10.1515/tnsci-2022-0256","url":null,"abstract":"Many diseases affect the autonomous nervous system and the central nervous system simultaneously, for example Parkinson's disease or irritable bowel syndrome. To study neurophysiologic interactions between the intestinal electrical activity and the electroencephalography (EEG) pattern of the brain, we combined intestinal electrical stimulation (IES) and non-invasive telemetric full-band DC EEG recordings in an acute pig-model. Intestinal motility was monitored with accelerometers. Brain activity was analyzed with regard to network driven phenomena like phase amplitude coupling (PAC) within two time-windows: 1 min after IES (early response) and 3 min after stimulation (late response). Here we present the results for two stimulation sites (small intestine, colon) and two parietal scalp-EEG channels (right and left somatosensory cortex region). Electrical stimulation consisted of a 30 or 130 Hz pulse. In summary, the PAC modulation index at a parietal EEG recording position is decreased after IES. This effect is in line with an inhibitory effect of our IES protocol regarding peristalsis. The surprisingly strong effects of IES on network driven EEG patterns may be translated into new therapeutic techniques and/or diagnostic tools in the future. Furthermore, analytic tools, operating on sparse datasets, may be ideally suited for the integration in implantable intestinal pacemakers as feedback system.","PeriodicalId":23227,"journal":{"name":"Translational Neuroscience","volume":"13 1","pages":"440-452"},"PeriodicalIF":1.8,"publicationDate":"2022-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9730545/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10421520","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Erratum to “Spinocerebellar ataxia type 40: A case report and literature review” 《脊髓小脑共济失调40型1例报告及文献复习》勘误

IF 2.1 4区医学

Translational Neuroscience Pub Date : 2022-01-01 DOI: 10.1515/tnsci-2022-0216

Fengyue Han, D. Su, C. Qu

引用次数: 0

Single-cell analysis of gene expression in the substantia nigra pars compacta of a pesticide-induced mouse model of Parkinson’s disease 农药诱导的帕金森病小鼠模型黑质致密部基因表达的单细胞分析

IF 2.1 4区医学

Translational Neuroscience Pub Date : 2022-01-01 DOI: 10.1101/2022.02.18.481079

Arshad H. Khan, Lydia K. Lee, Desmond J. Smith

引用次数: 1

Pre-ischemic exercise prevents inflammation and apoptosis by inhibiting MAPK pathway in ischemic stroke. 缺血前运动通过抑制MAPK通路预防缺血性卒中的炎症和细胞凋亡。

IF 2.1 4区医学

Translational Neuroscience Pub Date : 2022-01-01 DOI: 10.1515/tnsci-2022-0268

Zhen-Kun Gao, Xin-Ya Shen, Yu Han, Yi-Sha Guo, Kai Li, Xia Bi

{"title":"Pre-ischemic exercise prevents inflammation and apoptosis by inhibiting MAPK pathway in ischemic stroke.","authors":"Zhen-Kun Gao, Xin-Ya Shen, Yu Han, Yi-Sha Guo, Kai Li, Xia Bi","doi":"10.1515/tnsci-2022-0268","DOIUrl":"https://doi.org/10.1515/tnsci-2022-0268","url":null,"abstract":"Introduction: Mitogen-activated protein kinase (MAPK) pathway is a major mechanism of acute brain damage in ischemic stroke. Pre-ischemic exercise is an effective method to reduce ischemic injury. However, the regulation by pre-ischemic exercise of MAPK pathway and associated mechanisms in animal models remains unclear.Materials and methods: In this study, Male SD rats were randomly divided into sham group, middle cerebral artery occlusion (MCAO) group, and exercise plus MCAO (EX + MCAO) group for 21 days, and then was established by MCAO. Longa score was used to measure neurological deficits at 0, 1, 2, and 3 days after MCAO. Hematoxylin and eosin staining was used to observe the brain injury. The expression of MAPK pathway was quantified by western blot. The M1 microglia protein was quantified by western blot and immunofluorescence, and the level of inflammatory factor was measured by enzyme-linked immunosorbent assay. TUNEL staining and western blot were used to measure apoptosis.Results: In the current study, we observed that pre-ischemic exercise effectively decreased infarct volume, neurological deficit score and brain injury in MCAO rats through suppressing the activation of p-JNK and p-ERK1/2. Further investigation revealed that pre-ischemic exercise decreased M1 microglia activation and the serum level of TNF-α and IL-1β. In addition, the increased number of TUNEL-positive cells and Bax/Bcl-2 ratio also were reversed by pre-ischemic exercise.Conclusions: Pre-ischemic exercise can alleviate inflammatory response and apoptosis by inhibiting the MAPK pathway in MCAO rats.","PeriodicalId":23227,"journal":{"name":"Translational Neuroscience","volume":"13 1","pages":"495-505"},"PeriodicalIF":2.1,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9803980/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9091802","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mild acute stress prevents the memory impairment induced by long-term isoflurane anesthesia. 轻度急性应激可预防长期异氟醚麻醉引起的记忆损伤。

IF 2.1 4区医学

Translational Neuroscience Pub Date : 2022-01-01 DOI: 10.1515/tnsci-2022-0261

Tiantian Liu, Yutong Dai, Minhui Xu, Ying Chen, Tianjiao Xia, Xin Zhao

{"title":"Mild acute stress prevents the memory impairment induced by long-term isoflurane anesthesia.","authors":"Tiantian Liu, Yutong Dai, Minhui Xu, Ying Chen, Tianjiao Xia, Xin Zhao","doi":"10.1515/tnsci-2022-0261","DOIUrl":"https://doi.org/10.1515/tnsci-2022-0261","url":null,"abstract":"Objectives: Long-term isoflurane anesthesia exposure could result in postoperative cognitive dysfunction (POCD). Preoperative stress is also reported to be a risk factor of POCD. However, it is unknown whether acute stress could impair memory after long-term isoflurane anesthesia.Methods: In this study, we categorized the mice with acute stress into mild (30 min restraint stress), moderate (60 min restraint stress), and severe (120 min restraint stress) stress groups and then we used Open-Field Test (OFT) to detect whether different scales of acute restraint stress successfully induced acute stress in mice. The memory performance of mice was measured using contextual and cued memory test, and the brain-derived neurotrophic factor protein levels of hippocampus was detected by Western blot.Results: We verified that mild stress has pro-cognitive effect, but severe stress has amnestic effect. Moreover, we found that mild and moderate other than severe acute stress could partially attenuate the memory impairment induced by long-term isoflurane anesthesia.Conclusion: Mild and moderate acute stress could partially attenuate the memory impairment induced by long-term isoflurane anesthesia.","PeriodicalId":23227,"journal":{"name":"Translational Neuroscience","volume":"13 1","pages":"421-429"},"PeriodicalIF":2.1,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9719393/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10673642","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Longitudinal PET studies of mGluR5 in FXS using an FMR1 knockout mouse model 使用FMR1敲除小鼠模型对FXS中的mGluR5进行纵向PET研究

IF 2.1 4区医学

Translational Neuroscience Pub Date : 2022-01-01 DOI: 10.1515/tnsci-2022-0217

S. Afshar, S. Lule, Gengyang Yuan, Xiying Qu, C. Pan, M. Whalen, A. Brownell, M. Mody

{"title":"Longitudinal PET studies of mGluR5 in FXS using an FMR1 knockout mouse model","authors":"S. Afshar, S. Lule, Gengyang Yuan, Xiying Qu, C. Pan, M. Whalen, A. Brownell, M. Mody","doi":"10.1515/tnsci-2022-0217","DOIUrl":"https://doi.org/10.1515/tnsci-2022-0217","url":null,"abstract":"Abstract Fragile X syndrome (FXS) is a monogenic disorder characterized by intellectual disability and behavioral challenges. It is caused by aberrant methylation of the fragile X mental retardation 1 (FMR1) gene. Given the failure of clinical trials in FXS and growing evidence of a role of metabotropic glutamate subtype 5 receptors (mGluR5) in the pathophysiology of the disorder, we investigated mGluR5 function in FMR1 Knockout (FMR1-KO) mice and age- and sex-matched control mice using longitudinal positron emission tomography (PET) imaging to better understand the disorder. The studies were repeated at four time points to examine age- and disease-induced changes in mGluR5 availability using 3-fluoro-[18F]5-(2-pyridinylethynyl)benzonitrile ([18F]FPEB). We found that the binding potential (BP) of [18F]FPEB was significantly lower in the KO mice in mGluR5-implicated brain areas including striatum, cortex, hippocampus, thalamus, and olfactory bulb. The BP also changed with age, regardless of disorder status, increasing in early adulthood in male but not in female mice before decreasing later in both sexes. The difference in mGluR5 availability between the FMR1-KO and control mice and the change in BP in the KO mice as a function of age and sex illustrate the nature of the disorder and its progression, providing mechanistic insights for treatment design.","PeriodicalId":23227,"journal":{"name":"Translational Neuroscience","volume":"89 1","pages":"80 - 92"},"PeriodicalIF":2.1,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73639772","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3