Neuroscience最新文献

{"title":"Cell surface receptor-mediated signaling in CNS regeneration","authors":"Xinyu Liu ,&nbsp;Xiaofeng Zhao ,&nbsp;Mengsheng Qiu ,&nbsp;Junlin Yang","doi":"10.1016/j.neuroscience.2024.10.049","DOIUrl":"10.1016/j.neuroscience.2024.10.049","url":null,"abstract":"<div><div>Degenerative diseases and injuries of central nervous system (CNS) often cause nerve cell apoptosis and neural dysfunction. Protection of surviving cells or inducing the differentiation of stem cells into functional cells is considered to be an important way of neurorepair. In addition, transdifferentiation technology emerged recently is expected to provide new solutions for nerve regeneration. Cell surface receptors are transmembrane proteins embedded in cytoplasmic membrane, and play crucial roles in maintaining communication between extracellular signals and intracellular signaling processes. The extracellular microenvironment changed dramatically upon neural lesion, exploring the biological function of signals mediated by cell surface receptors will help to develop molecular strategies for nerve regeneration. An increasing number of studies have reported that cell surface receptor-mediated signaling affects the survival, differentiation, and functioning of neural cells, and even regulate their <em>trans</em>-lineage reprogramming. Here, we provide a review on the roles of cell surface receptors in CNS regeneration, thus providing new cues for better treatment of neurodegenerative diseases or nerve injury.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"562 ","pages":"Pages 198-208"},"PeriodicalIF":2.9,"publicationDate":"2024-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142564805","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Selective blockade of cannabinoid receptors influence motoneuron survival and glial reaction after neonatal axotomy.","authors":"Matheus Perez, Aline Barroso Spejo, Gabriela Bortolança Chiarotto, Francisco Silveira Guimarães, Alexandre Leite Rodrigues de Oliveira, Luciana Politti Cartarozzi","doi":"10.1016/j.neuroscience.2024.10.051","DOIUrl":"https://doi.org/10.1016/j.neuroscience.2024.10.051","url":null,"abstract":"<p><p>Sciatic nerve crush in neonatal rats leads to an extensive death of motor and sensory neurons, serving as a platform to develop new neuroprotective approaches. The endocannabinoid system plays important neuromodulatory roles and has been involved in neurodevelopment and neuroprotection. The present work investigated the role of the cannabinoid receptors CB1 and CB2 in the neuroprotective response after neonatal axotomy. CB1 and CB2 antagonists (AM251 and AM630, respectively) were used after sciatic nerve crush in 2-day-old Wistar rats. Five days after lesion and treatment, the rats were perfused, and the spinal cords and dorsal root ganglia (DRG) were obtained and processed to investigate neuronal survival and immunohistochemistry changes, or RT-qPCR analysis. Motoneuron survival analysis showed that blocking CB2 alone or in combination with CB1 was neuroprotective. This effect was associated with a decrease in astrogliosis and microglial reaction. Interestingly, Cnr1 (CB1) and Bdnf gene transcripts were downregulated in the spinal cords of the antagonist-treated groups. Despite no intergroup difference regarding neuronal survival in the DRG, the simultaneous blockade of CB1 and CB2 receptors led to an increased expression of both Cnr1 and Cnr2, combined with Gdnf upregulation. The results indicate that the selective antagonism of cannabinoid receptors facilitates neuroprotection and decreases glial reactivity, suggesting new potential treatment approaches.</p>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142558328","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Renshaw cells, corelease and nicotinic receptors: The last journey in synaptic transmission.","authors":"Boris Lamotte d'Incamps","doi":"10.1016/j.neuroscience.2024.10.041","DOIUrl":"10.1016/j.neuroscience.2024.10.041","url":null,"abstract":"<p><p>Philippe Ascher spent his last two decades as an emeritus Professor, working in the heart of Paris. Together with his wife Jacsue they were hosted in Alain Marty's laboratory and enjoyed the happiest retirement. We started our collaboration a few years after they started their retirement research at the Saint Pères campus where I was working on spinal motoneurons' physiology. This period led us from NMDA receptors to the corelease of acetylcholine and glutamate by spinal motoneurons to Renshaw cells and then to the stoichiometric variants of nicotinic acetylcholine receptors. Here I present a brief history of our collaboration during this period.</p>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142550079","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microdosing of a kappa opioid receptor agonist within proximal nucleus accumbens shell microstructures revealing opposing behavioral outcomes","authors":"Erin B. Rousseau ,&nbsp;Hannah D. Jackson ,&nbsp;Suman Guha ,&nbsp;Sydney S. Sherman ,&nbsp;Michael Cima ,&nbsp;Elena H. Chartoff","doi":"10.1016/j.neuroscience.2024.10.047","DOIUrl":"10.1016/j.neuroscience.2024.10.047","url":null,"abstract":"<div><div>Targeted intracranial delivery of molecularly-specific therapies within intricate brain structures poses a formidable challenge due to the heterogeneity of neuronal phenotypes and functions. Here we report the use of an implantable, miniaturized neural drug delivery system permitting dynamic adjustment of pharmacotherapies. Specifically, we exploit the spatial accuracy afforded by this method for targeting modulation of neuronal microstructures. Kappa opioid receptors (KOR) within the dorsal medial nucleus accumbens shell (NASh) are selectively activated through micro infusions of the KOR agonist, U-50488. Remarkably, we demonstrate that micro infusions of U-50488 into the dorsal NASh induces reward-like conditioned place preferences, whereas a mere 1 mm shift ventrally results in conditioned place aversions. The striking precision afforded by this method may prove useful in other neurotherapeutic interventions.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"563 ","pages":"Pages 261-267"},"PeriodicalIF":2.9,"publicationDate":"2024-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142567509","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “Assessing the location, relative expression and subclass of dopamine receptors in the cerebellum of hemi-parkinsonian rats” [Neuroscience 521 (2023) 1–19]","authors":"Emily C. Mahoney-Rafferty ,&nbsp;Heidi R. Tucker ,&nbsp;Kainat Akhtar ,&nbsp;Rachael Herlihy ,&nbsp;Aliyah Audil ,&nbsp;Dia Shah ,&nbsp;Megan Gupta ,&nbsp;Eliyahu M. Kochman ,&nbsp;Paul J. Feustel ,&nbsp;Eric S. Molho ,&nbsp;Julie G. Pilitsis ,&nbsp;Damian S. Shin","doi":"10.1016/j.neuroscience.2024.10.044","DOIUrl":"10.1016/j.neuroscience.2024.10.044","url":null,"abstract":"","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"562 ","pages":"Page 63"},"PeriodicalIF":2.9,"publicationDate":"2024-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142552573","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Natural and bio-engineered stem cell-derived extracellular vesicles for spinal cord injury repair: A meta-analysis with trial sequential analysis","authors":"Hankun Su ,&nbsp;Yixin Chen ,&nbsp;Boya Tang ,&nbsp;Fen Xiao ,&nbsp;Yuanyuan Sun ,&nbsp;Jingjing Chen ,&nbsp;Li Deng ,&nbsp;Aihua He ,&nbsp;Ge Li ,&nbsp;Yan Luo ,&nbsp;Hui Li","doi":"10.1016/j.neuroscience.2024.10.018","DOIUrl":"10.1016/j.neuroscience.2024.10.018","url":null,"abstract":"<div><h3>Background</h3><div>Stem-cell derived extracellular vesicles (EVs) have shown promise in preclinical spinal cord injury (SCI) models but lack a comprehensive literature review for clinical translation guidance.</div></div><div><h3>Methods</h3><div>This <em>meta</em>-analysis with trial sequential analysis systematically search PubMed, Web of Science, Embase, and Cochrane Library databases. Prespecified inclusion criteria were studies reporting on measurable outcomes relevant to SCI repair. Risk of bias and quality of reporting were assessed. Random-effects <em>meta</em>-analyses and subgroup analyses comparing natural and bio-engineered EVs were performed. The study was registered with PROSPERO (CRD42024512122).</div></div><div><h3>Findings</h3><div>The search identified 3935 records, of which 39 studies were included, totaling 1801 animals. Administration of EVs significantly improved locomotor function as measured by Basso-Beattie-Bresnahan or Basso-Mouse-Scale scores at 1 week (natural EVs: SMD 1.50, 95 % CI 1.06–1.95; bio-engineered EVs: SMD 1.93, 95 % CI 1.34–2.52) and 3 weeks (natural EVs: SMD 2.57, 95 % CI 1.96–3.17; bio-engineered EVs: SMD 3.16, 95 % CI 2.29–4.02) post-injury. Subgroup analyses indicated surface modification approaches were most effective among bio-engineered EV strategies. EVs also promoted nerve growth (SMD 2.95, 95 % CI 2.12–3.78), enhanced neuron conductivity (MD 0.75, 95 %CI 0.59–0.90), alleviated inflammation (SMD −3.12, 95 % CI −4.15--2.10), and reduced lesion size (SMD −2.90, 95 % CI −3.87--1.93).</div></div><div><h3>Conclusions</h3><div>Both natural and bio-engineered EVs improve functional and pathological outcomes in animal models of SCI. The enhanced benefits observed with bio-engineered EVs, particularly those utilizing surface modification approaches, highlight the importance of continued exploration into bio-engineering techniques to optimize EVs’ therapeutic efficacy for SCI repair.</div><div><strong>Protocol Registration</strong></div><div>CRD42024512122.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"562 ","pages":"Pages 135-147"},"PeriodicalIF":2.9,"publicationDate":"2024-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142567685","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nanostructured Photonics Probes: A Transformative Approach in Neurotherapeutics and Brain Circuitry","authors":"Bakr Ahmed Taha ,&nbsp;Ali J. Addie ,&nbsp;Ali Q Saeed ,&nbsp;Adawiya J. Haider ,&nbsp;Vishal Chaudhary ,&nbsp;Norhana Arsad","doi":"10.1016/j.neuroscience.2024.10.046","DOIUrl":"10.1016/j.neuroscience.2024.10.046","url":null,"abstract":"<div><div>Neuroprobes that use nanostructured photonic interfaces are capable of multimodal sensing, stimulation, and imaging with unprecedented spatio-temporal resolution. In addition to electrical recording, optogenetic modulation, high-resolution optical imaging, and molecular sensing, these advanced probes combine nanophotonic waveguides, optical transducers, nanostructured electrodes, and biochemical sensors. The potential of this technology lies in unraveling the mysteries of neural coding principles, mapping functional connectivity in complex brain circuits, and developing new therapeutic interventions for neurological disorders. Nevertheless, achieving the full potential of nanostructured photonic neural probes requires overcoming challenges such as ensuring long-term biocompatibility, integrating nanoscale components at high density, and developing robust data-analysis pipelines. In this review, we summarize and discuss the role of photonics in neural probes, trends in electrode diameter for neural interface technologies, nanophotonic technologies using nanostructured materials, advances in nanofabrication photonics interface engineering, and challenges and opportunities. Finally, interdisciplinary efforts are required to unlock the transformative potential of next-generation neuroscience therapies.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"562 ","pages":"Pages 106-124"},"PeriodicalIF":2.9,"publicationDate":"2024-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142560751","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroglobin protects dopaminergic neurons in a Parkinson’s cell model by interacting with mitochondrial complex NDUFA10","authors":"Xiaomei Liang ,&nbsp;Yutong Wen ,&nbsp;Cuilian Feng ,&nbsp;Lan Xu ,&nbsp;Ying Xian ,&nbsp;Haiting Xie ,&nbsp;Jianou Huang ,&nbsp;Yihong Huang ,&nbsp;Xiaodong Zhao ,&nbsp;Xiaoya Gao","doi":"10.1016/j.neuroscience.2024.10.033","DOIUrl":"10.1016/j.neuroscience.2024.10.033","url":null,"abstract":"<div><div>The study aimed to validate the protective effect of neuroglobin (Ngb) in a cell model of Parkinson’s disease (PD) and explore its therapeutic potential. Lentivirus-Ngb (LvNgb) and siRNA-Ngb (siNgb) were used to achieve Ngb overexpression and knockdown, respectively, in a sporadic PD cell model. Apoptosis was evaluated by flow cytometry-based Annexin V/propidium iodide assays. Activation of the pro-apoptotic factor, Caspase-9, was detected by immunoblotting, and Complex I activities were detected by using enzyme-linked immunosorbent assay (ELISA). Mitochondrial dysfunction was examined by measuring the mitochondrial membrane potential (MMP), NAD⁺/NADH ratios, and reactive oxygen species (ROS) levels. Additionally, coimmunoprecipitation (Co-IP) assays were conducted in mouse neuroblastoma cell line 9D (MN9D) cells to determine the interactions of Ngb with the Complex I subunit NDUFA10. The results showed that Ngb overexpression reduced the percentages of apoptotic cells, total caspase-9 levels and restored Complex I activities in the PD cell model. Conversely, knockdown of Ngb resulted in an increase in apoptotic cells, higher total caspase-9 levels, and decreased Complex I activities. Furthermore, Ngb overexpression restored MMP and NAD⁺/NADH ratios and alleviated ROS-mediated oxidative stress in MN9D cells. Finally, Co-IP confirmed the interaction between Ngb and NDUFA10 in MN9D cells. In conclusion, Ngb protects MN9D cells against apoptosis by interacting with Complex I subunit NDUFA10, rescuing its activity and inhibiting the mitochondrial pathway of apoptosis in the MPP⁺-mediated PD model.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"562 ","pages":"Pages 43-53"},"PeriodicalIF":2.9,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142504862","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Frequent absent mindedness and the neural mechanism trapped by mobile phone addiction","authors":"Jingjing Zhang ,&nbsp;Qiuyang Feng ,&nbsp;Jiang Qiu","doi":"10.1016/j.neuroscience.2024.10.042","DOIUrl":"10.1016/j.neuroscience.2024.10.042","url":null,"abstract":"<div><div>With the increased availability and sophistication of digital devices in the last decade, young people have become mainstream mobile phone users. Heavy mobile phone dependence causes affective problems (depression, anxiety) and loss of attention on current activities, leading to more cluttered thoughts. Problematic mobile phone use has been found to increase the occurrence of mind wandering, but the neural mechanism underlying this relationship remains unclear. The current study aims to investigate the neural mechanism between mobile phone use and mind wandering. University students from datasets (ongoing research project named Gene-Brain-Behavior project, GBB) completed psychological assessments of mobile phone addiction and mind wandering and underwent resting-state functional connectivity (FC) scanning. FC matrix was constructed to further conduct correlation and mediation analyses. Students with high mobile phone addiction scores were more likely to have high mind wandering scores. FC among the default mode, motor, frontoparietal, basal ganglia, limbic, medial frontal, visual association, and cerebellar networks formed the neural basis of mind wandering. FC between the frontoparietal and motor networks, between the default mode network and cerebellar network, and within the cerebellar network mediated the relationship between mobile phone addiction and mind wandering. The findings confirm that mobile phone addiction is a risk factor for increased mind wandering and reveal that FC in several brain networks underlies this relationship. They contribute to research on behavioral addiction, education, and mental health among young adults.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"563 ","pages":"Pages 252-260"},"PeriodicalIF":2.9,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142504848","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"METTL3 inhibits microglial pyroptosis in neonatal hypoxia-ischemia encephalopathy by regulating GPR39 expression in an m6A-HuR-dependent manner","authors":"Xili Jiang ,&nbsp;Wei Zhang ,&nbsp;Shucai Xie","doi":"10.1016/j.neuroscience.2024.10.038","DOIUrl":"10.1016/j.neuroscience.2024.10.038","url":null,"abstract":"<div><h3>Background</h3><div>Neonatal hypoxia–ischemia encephalopathy (HIE) is a significant reason for neonatal mortality and prolonged disability. We have previously revealed that GPR39 activation attenuates neuroinflammation in a neonatal HIE rat model. This study aimed to investigate whether GPR39 affected microglial pyroptosis post-HIE.</div></div><div><h3>Methods</h3><div>A neonatal rat model of HIE and a microglia cell model of oxygen-glucose deprivation (OGD) were established. Neuronal loss and cerebral infarction were assessed by using TTC, H&amp;E staining, and Nissl staining. Pyroptosis was evaluated with western blot, LDH assay kit, ELISA, and flow cytometry. Total m6A level and GPR39 m6A modification were determined using m6A dot blot and MeRIP. The interaction between METTL3/HuR/GSK3β and GPR39 was analyzed by performing molecular interaction experiments. GPR39 mRNA stability was examined with actinomycin D.</div></div><div><h3>Results</h3><div>The level of GPR39 was increased in neonatal HIE rats and OGD-treated microglia. Brain injury and neuronal loss were significantly increased in the HIE model when GPR39 was knocked down. GPR39 knockdown aggravated NLRP3 inflammasome-mediated microglial pyroptosis. METTL3 upregulated GPR39 expression in an m6A-dependent manner. METTL3 enhanced the interaction of HuR and GPR39. In OGD-exposed microglia, METTL3 elevated GPR39 expression and mRNA stability, which declined after HuR depletion. METTL3 knockdown promoted microglial pyroptosis, which was reversed by GPR39 agonist. Furthermore, microglial pyroptosis was inhibited by GPR39 upregulation, but the outcome was reverted by GSK3β activator SNP.</div></div><div><h3>Conclusion</h3><div>METTL3 inhibits microglial pyroptosis in neonatal HIE via regulating m6A-HuR dependent stabilization of GPR39, which contributes to therapeutics development for neonatal HIE.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"563 ","pages":"Pages 175-187"},"PeriodicalIF":2.9,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142504860","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}