ASN NEURO最新文献_第4页

Pyruvate Kinase 2, an Energy Metabolism Related Enzyme, May Have a Neuroprotective Function in Retinal Degeneration. 丙酮酸激酶2，一种能量代谢相关酶，可能在视网膜变性中具有神经保护功能。

IF 4.7 4区医学

ASN NEURO Pub Date : 2023-01-01 DOI: 10.1177/17590914231151534

Jiaming Zhou, Per Ekström

{"title":"Pyruvate Kinase 2, an Energy Metabolism Related Enzyme, May Have a Neuroprotective Function in Retinal Degeneration.","authors":"Jiaming Zhou, Per Ekström","doi":"10.1177/17590914231151534","DOIUrl":"https://doi.org/10.1177/17590914231151534","url":null,"abstract":"Retinitis pigmentosa (RP) is an inherited disorder that results in vision impairment but general and mutation-independent therapeutic strategies are not available. However, it is widely regarded that the cGMP system, including cGMP and its interactor cGMP-dependent protein kinase (PKG), acts as a crucial effector during retinal degeneration. We have previously identified a list of cGMP-PKG-dependent genes in the context of RP, and in this study, we further validated one of these, namely pyruvate kinase 2 (PKM2), and investigated the potential role of PKM2 for the photoreceptors' well-being during RP. With the aid of organotypic retinal explant cultures, we pharmacologically manipulated the PKM2 activities in two different RP mouse models (rd2 and rd10) via the addition of TEPP-46 (a PKM2 activator) and found that activation of PKM2 alleviates the progress of photoreceptor death in the rd10 mouse model. We also noted that the expression of both PKM2 and one of its targets, glucose transporter-1 (Glut1), showed alterations depending on the degeneration state. The observations provide supportive evidence that PKM2 may serve as a novel potential molecular target in RP.","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"15 ","pages":"17590914231151534"},"PeriodicalIF":4.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9376862","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: 0

Neuroinflammation: The Abused Concept. 神经炎：滥用的概念。

IF 4.7 4区医学

ASN NEURO Pub Date : 2023-01-01 DOI: 10.1177/17590914231197523

Elena Galea, Manuel B Graeber

{"title":"Neuroinflammation: The Abused Concept.","authors":"Elena Galea, Manuel B Graeber","doi":"10.1177/17590914231197523","DOIUrl":"10.1177/17590914231197523","url":null,"abstract":"Scientific progress requires the relentless correction of errors and refinement of hypotheses. Clarity of terminology is essential for clarity of thought and proper experimental interrogation of nature. Therefore, the application of the same scientific term to different and even conflicting phenomena and concepts is not useful and must be corrected. Such abuse of terminology has happened and is still increasing in the case of \"neuroinflammation,\" a term that until the 1990s meant classical inflammation affecting the central nervous system (CNS) and thereon was progressively used to mostly denote microglia activation. The resulting confusion is very wasteful and detrimental not only for scientists but also for patients, given the numerous failed clinical trials in acute and chronic CNS diseases over the last decade with \"anti-inflammatory\" drugs. Despite this failure, reassessments of the \"neuroinflammation\" concept are rare, especially considering the number of articles still using the term. This undesirable situation motivates this article. We review the origins and evolution of the term \"neuroinflammation,\" discuss the unique tissue defense and repair strategies in the CNS, define CNS immunity, and emphasize the notion of gliopathies to help readdress, if not bury, the term \"neuroinflammation\" as it stands in the way of scientific progress.","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"15 ","pages":"17590914231197523"},"PeriodicalIF":4.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/9b/cb/10.1177_17590914231197523.PMC10469255.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10509490","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

How Oxidative Stress Induces Depression? 氧化应激如何诱发抑郁?

IF 4.7 4区医学

ASN NEURO Pub Date : 2023-01-01 DOI: 10.1177/17590914231181037

Na Ji, Mengzhu Lei, Yating Chen, Shaowen Tian, Chuanyu Li, Bo Zhang

{"title":"How Oxidative Stress Induces Depression?","authors":"Na Ji, Mengzhu Lei, Yating Chen, Shaowen Tian, Chuanyu Li, Bo Zhang","doi":"10.1177/17590914231181037","DOIUrl":"https://doi.org/10.1177/17590914231181037","url":null,"abstract":"Depression increasingly affects a wide range and a large number of people worldwide, both physically and psychologically, which makes it a social problem requiring prompt attention and management. Accumulating clinical and animal studies have provided us with substantial insights of disease pathogenesis, especially central monoamine deficiency, which considerably promotes antidepressant research and clinical treatment. The first-line antidepressants mainly target the monoamine system, whose drawbacks mainly include slow action and treatment resistant. The novel antidepressant esketamine, targeting on central glutamatergic system, rapidly and robustly alleviates depression (including treatment-resistant depression), whose efficiency is shadowed by potential addictive and psychotomimetic side effects. Thus, exploring novel depression pathogenesis is necessary, for seeking more safe and effective therapeutic methods. Emerging evidence has revealed vital involvement of oxidative stress (OS) in depression, which inspires us to pursue antioxidant pathway for depression prevention and treatment. Fully uncovering the underlying mechanisms of OS-induced depression is the first step towards the avenue, thus we summarize and expound possible downstream pathways of OS, including mitochondrial impairment and related ATP deficiency, neuroinflammation, central glutamate excitotoxicity, brain-derived neurotrophic factor/tyrosine receptor kinase B dysfunction and serotonin deficiency, the microbiota-gut-brain axis disturbance and hypothalamic-pituitary-adrenocortical axis dysregulation. We also elaborate on the intricate interactions between the multiple aspects, and molecular mechanisms mediating the interplay. Through reviewing the related research progress in the field, we hope to depict an integral overview of how OS induces depression, in order to provide fresh ideas and novel targets for the final goal of efficient treatment of the disease.","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"15 ","pages":"17590914231181037"},"PeriodicalIF":4.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/0d/c1/10.1177_17590914231181037.PMC10280786.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10065729","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

Astrocyte and Neuronal Panx1 Support Long-Term Reference Memory in Mice. 星形胶质细胞和神经元Panx1支持小鼠长期参考记忆。

IF 4.7 4区医学

ASN NEURO Pub Date : 2023-01-01 DOI: 10.1177/17590914231184712

Price Obot, Galadu Subah, Antonia Schonwald, Jian Pan, Libor Velíšek, Jana Velíšková, Patric K Stanton, Eliana Scemes

{"title":"Astrocyte and Neuronal Panx1 Support Long-Term Reference Memory in Mice.","authors":"Price Obot, Galadu Subah, Antonia Schonwald, Jian Pan, Libor Velíšek, Jana Velíšková, Patric K Stanton, Eliana Scemes","doi":"10.1177/17590914231184712","DOIUrl":"https://doi.org/10.1177/17590914231184712","url":null,"abstract":"Pannexin 1 (Panx1) is an ubiquitously expressed protein that forms plasma membrane channels permeable to anions and moderate-sized signaling molecules (e.g., ATP, glutamate). In the nervous system, activation of Panx1 channels has been extensively shown to contribute to distinct neurological disorders (epilepsy, chronic pain, migraine, neuroAIDS, etc.), but knowledge of the extent to which these channels have a physiological role remains restricted to three studies supporting their involvement in hippocampus dependent learning. Given that Panx1 channels may provide an important mechanism for activity-dependent neuron-glia interaction, we used Panx1 transgenic mice with global and cell-type specific deletions of Panx1 to interrogate their participation in working and reference memory. Using the eight-arm radial maze, we show that long-term spatial reference memory, but not spatial working memory, is deficient in Panx1-null mice and that both astrocyte and neuronal Panx1 contribute to the consolidation of long-term spatial memory. Field potential recordings in hippocampal slices of Panx1-null mice revealed an attenuation of both long-term potentiation (LTP) of synaptic strength and long-term depression (LTD) at Schaffer collateral-CA1 synapses without alterations of basal synaptic transmission or pre-synaptic paired-pulse facilitation. Our results implicate both neuronal and astrocyte Panx1 channels as critical players for the development and maintenance of long-term spatial reference memory in mice.","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"15 ","pages":"17590914231184712"},"PeriodicalIF":4.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/1d/58/10.1177_17590914231184712.PMC10326369.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9766071","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

The Initial Myelination in the Central Nervous System. 中枢神经系统的初始髓鞘形成。

IF 4.7 4区医学

ASN NEURO Pub Date : 2023-01-01 DOI: 10.1177/17590914231163039

Qiang Yu, Teng Guan, Ying Guo, Jiming Kong

{"title":"The Initial Myelination in the Central Nervous System.","authors":"Qiang Yu, Teng Guan, Ying Guo, Jiming Kong","doi":"10.1177/17590914231163039","DOIUrl":"https://doi.org/10.1177/17590914231163039","url":null,"abstract":"Myelination contributes not only to the rapid nerve conduction but also to axonal insulation and protection. In the central nervous system (CNS), the initial myelination features a multistep process where oligodendrocyte precursor cells undergo proliferation and migration before differentiating into mature oligodendrocytes. Mature oligodendrocytes then extend processes and wrap around axons to form the multilayered myelin sheath. These steps are tightly regulated by various cellular and molecular mechanisms, such as transcription factors (Olig family, Sox family), growth factors (PDGF, BDNF, FGF-2, IGF), chemokines/cytokines (TGF-β, IL-1β, TNFα, IL-6, IFN-γ), hormones (T3), axonal signals (PSA-NCAM, L1-CAM, LINGO-1, neural activity), and intracellular signaling pathways (Wnt/β-catenin, PI3 K/AKT/mTOR, ERK/MAPK). However, the fundamental mechanisms for initial myelination are yet to be fully elucidated. Identifying pivotal mechanisms for myelination onset, development, and repair will become the focus of future studies. This review focuses on the current understanding of how CNS myelination is initiated and also the regulatory mechanisms underlying the process.","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"15 ","pages":"17590914231163039"},"PeriodicalIF":4.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/c5/0c/10.1177_17590914231163039.PMC10052612.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9884819","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

Regulation of the Volume-Regulated Anion Channel Pore-Forming Subunit LRRC8A in the Intrahippocampal Kainic Acid Model of Mesial Temporal Lobe Epilepsy. 体积调节阴离子通道成孔亚基LRRC8A在内侧颞叶癫痫海马内凯尼克酸模型中的调控作用。

IF 4.7 4区医学

ASN NEURO Pub Date : 2023-01-01 DOI: 10.1177/17590914231184072

Manolia R Ghouli, Carrie R Jonak, Rajan Sah, Todd A Fiacco, Devin K Binder

{"title":"Regulation of the Volume-Regulated Anion Channel Pore-Forming Subunit LRRC8A in the Intrahippocampal Kainic Acid Model of Mesial Temporal Lobe Epilepsy.","authors":"Manolia R Ghouli, Carrie R Jonak, Rajan Sah, Todd A Fiacco, Devin K Binder","doi":"10.1177/17590914231184072","DOIUrl":"10.1177/17590914231184072","url":null,"abstract":"Volume-regulated anion channels (VRACs) are a group of ubiquitously expressed outwardly-rectifying anion channels that sense increases in cell volume and act to return cells to baseline volume through an efflux of anions and organic osmolytes, including glutamate. Because cell swelling, increased extracellular glutamate levels, and reduction of the brain extracellular space (ECS) all occur during seizure generation, we set out to determine whether VRACs are dysregulated throughout mesial temporal lobe epilepsy (MTLE), the most common form of adult epilepsy. To accomplish this, we employed the IHKA experimental model of MTLE, and probed for the expression of LRRC8A, the essential pore-forming VRAC subunit, at acute, early-, mid-, and late-epileptogenic time points (1-, 7-, 14-, and 30-days post-IHKA, respectively). Western blot analysis revealed the upregulation of total dorsal hippocampal LRRC8A 14-days post-IHKA in both the ipsilateral and contralateral hippocampus. Immunohistochemical analyses showed an increased LRRC8A signal 7-days post-IHKA in both the ipsilateral and contralateral hippocampus, along with layer-specific changes 1-, 7-, and 30-days post-IHKA bilaterally. LRRC8A upregulation 1 day post-IHKA was observed primarily in astrocytes; however, some upregulation was also observed in neurons. Glutamate-GABA/glutamine cycle enzymes glutamic acid decarboxylase, glutaminase, and glutamine synthetase were also dysregulated at the 7-day timepoint post status epilepticus. The timepoint-dependent upregulation of total hippocampal LRRC8A and the possible subsequent increased efflux of glutamate in the epileptic hippocampus suggest that the dysregulation of astrocytic VRAC may play an important role in the development of epilepsy.","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"15 ","pages":"17590914231184072"},"PeriodicalIF":4.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/6e/15/10.1177_17590914231184072.PMC10331354.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10181528","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

All the PNS is a Stage: Transplanted Bone Marrow Cells Play an Immunomodulatory Role in Peripheral Nerve Regeneration. 所有PNS都是一个阶段：移植骨髓细胞在周围神经再生中发挥免疫调节作用。

IF 3.9 4区医学

ASN NEURO Pub Date : 2023-01-01 DOI: 10.1177/17590914231167281

Gonzalo Piñero, Marianela Vence, Marcos L Aranda, Magalí C Cercato, Paula A Soto, Vanina Usach, Patricia C Setton-Avruj

引用次数: 0

Müller Glia to Müller Glia Extracellular Vesicle-Dependent Signaling Induces Multipotency Genes Nestin and lin28 Expression in Response to N-methyl-D-aspartate (NMDA) Exposure. 神经胶质瘤与神经胶质瘤细胞外囊泡依赖信号传导诱导NMDA暴露后多能基因Nestin和lin28的表达

IF 4.7 4区医学

ASN NEURO Pub Date : 2023-01-01 DOI: 10.1177/17590914231183272

Ana Karen Carapia, Erick J Martinez-Colin, Deisy Segura-Villalobos, Rebeca Yael Victoria-Chavez, Ivonne Lezama, Eduardo Martinez-Martinez, Monica Lamas

引用次数: 0

The α₂ Adrenoceptor Agonist and Sedative/Anaesthetic Dexmedetomidine Excites Diverse Neuronal Types in the Ventrolateral Preoptic Area of Male Mice. α2肾上腺素受体激动剂和镇静/麻醉用右美托咪定刺激雄性小鼠视前腹外侧区不同类型的神经元。

IF 4.7 4区医学

ASN NEURO Pub Date : 2023-01-01 DOI: 10.1177/17590914231191016

Sumei Fan, Xinqi Cheng, Pingping Zhang, Yuanyin Wang, Liecheng Wang, Juan Cheng

引用次数: 0

Activation of the PACAP/PAC1 Signaling Pathway Accelerates the Repair of Impaired Spatial Memory Caused by an Ultradian Light Cycle. PACAP/PAC1信号通路的激活加速了超强光周期引起的空间记忆损伤的修复

IF 4.7 4区医学

ASN NEURO Pub Date : 2023-01-01 DOI: 10.1177/17590914231169140

Dejiao Xu, Ying Zhang, Jun Feng, Hongyu Fu, Jiayi Li, Wei Wang, Zhen Li, Pingping Zhang, Xinqi Cheng, Liecheng Wang, Juan Cheng

{"title":"Activation of the PACAP/PAC1 Signaling Pathway Accelerates the Repair of Impaired Spatial Memory Caused by an Ultradian Light Cycle.","authors":"Dejiao Xu, Ying Zhang, Jun Feng, Hongyu Fu, Jiayi Li, Wei Wang, Zhen Li, Pingping Zhang, Xinqi Cheng, Liecheng Wang, Juan Cheng","doi":"10.1177/17590914231169140","DOIUrl":"https://doi.org/10.1177/17590914231169140","url":null,"abstract":"The mechanism of light-induced spatial memory deficits, as well as whether rhythmic expression of the pituitary adenylyl cyclase-activating polypeptides (PACAP)-PAC1 pathway influenced by light is related to this process, remains unclear. Here, we aimed to investigate the role of the PACAP-PAC1 pathway in light-mediated spatial memory deficits. Animals were first housed under a T24 cycle (12 h light:12 h dark), and then light conditions were transformed to a T7 cycle (3.5 h light:3.5 h dark) for at least 4 weeks. The spatial memory function was assessed using the Morris water maze (MWM). In line with behavioral studies, rhythmic expression of the PAC1 receptor and glutamate receptors in the hippocampal CA1 region was assessed by western blotting, and electrophysiology experiments were performed to determine the influence of the PACAP-PAC1 pathway on neuronal excitability and synaptic signaling transmission. Spatial memory was deficient after mice were exposed to the T7 light cycle. Rhythmic expression of the PAC1 receptor was dramatically decreased, and the excitability of CA1 pyramidal cells was decreased in T7 cycle-housed mice. Compensation with PACAP1-38, a PAC1 receptor agonist, helped T7 cycle-housed mouse CA1 pyramidal cells recover neuronal excitability to normal levels, and cannulas injected with PACAP1-38 shortened the time to find the platform in MWM. Importantly, the T7 cycle decreased the frequency of AMPA receptor-mediated excitatory postsynaptic currents. In conclusion, the PACAP-PAC1 pathway is an important protective factor modulating light-induced spatial memory function deficits, affecting CA1 pyramidal cell excitability and excitatory synaptic signaling transmission.","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"15 ","pages":"17590914231169140"},"PeriodicalIF":4.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/a1/b4/10.1177_17590914231169140.PMC10123913.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9507389","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