scholarly journals Cellular and molecular mechanisms of axolotl central and peripheral nervous system response to injury

2018 ◽  
Author(s):  
Freitas
Keyword(s):  
Nervous System ◽  
Peripheral Nervous System ◽  
Molecular Mechanisms ◽  
System Response

scholarly journals Immune Actions on the Peripheral Nervous System in Pain

2021 ◽  
Vol 22 (3) ◽  
pp. 1448
Author(s):  
Jessica Aijia Liu ◽  
Jing Yu ◽  
Chi Wai Cheung
Keyword(s):  
Chronic Pain ◽  
Nervous System ◽  
Peripheral Nervous System ◽  
Immune Cells ◽  
Molecular Mechanisms ◽  
Process Integration ◽  
Current Knowledge ◽  
Therapeutic Strategies ◽  
Lipid Mediators ◽  
Cellular Changes

Pain can be induced by tissue injuries, diseases and infections. The interactions between the peripheral nervous system (PNS) and immune system are primary actions in pain sensitizations. In response to stimuli, nociceptors release various mediators from their terminals that potently activate and recruit immune cells, whereas infiltrated immune cells further promote sensitization of nociceptors and the transition from acute to chronic pain by producing cytokines, chemokines, lipid mediators and growth factors. Immune cells not only play roles in pain production but also contribute to PNS repair and pain resolution by secreting anti-inflammatory or analgesic effectors. Here, we discuss the distinct roles of four major types of immune cells (monocyte/macrophage, neutrophil, mast cell, and T cell) acting on the PNS during pain process. Integration of this current knowledge will enhance our understanding of cellular changes and molecular mechanisms underlying pain pathogenies, providing insights for developing new therapeutic strategies.

scholarly journals Identification of Candidate Genes Associated with Charcot-Marie-Tooth Disease by Network and Pathway Analysis

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Min Zhong ◽  
Qing Luo ◽  
Ting Ye ◽  
XiDan Zhu ◽  
Xiu Chen ◽  
...  
Keyword(s):  
Nervous System ◽  
Candidate Genes ◽  
Peripheral Nervous System ◽  
Molecular Mechanisms ◽  
Clinical Genetic ◽  
Systematic Analysis ◽  
Charcot Marie Tooth ◽  
Charcot Marie Tooth Disease ◽  
Functional Features ◽  
Tooth Disease

Charcot-Marie-Tooth Disease (CMT) is the most common clinical genetic disease of the peripheral nervous system. Although many studies have focused on elucidating the pathogenesis of CMT, few focuses on achieving a systematic analysis of biology to decode the underlying pathological molecular mechanisms and the mechanism of its disease remains to be elucidated. So our study may provide further useful insights into the molecular mechanisms of CMT based on a systematic bioinformatics analysis. In the current study, by reviewing the literatures deposited in PUBMED, we identified 100 genes genetically related to CMT. Then, the functional features of the CMT-related genes were examined by R software and KOBAS, and the selected biological process crosstalk was visualized with the software Cytoscape. Moreover, CMT specific molecular network analysis was conducted by the Molecular Complex Detection (MCODE) Algorithm. The biological function enrichment analysis suggested that myelin sheath, axon, peripheral nervous system, mitochondrial function, various metabolic processes, and autophagy played important roles in CMT development. Aminoacyl-tRNA biosynthesis, metabolic pathways, and vasopressin-regulated water reabsorption were significantly enriched in the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway network, suggesting that these pathways may play key roles in CMT occurrence and development. According to the crosstalk, the biological processes could be roughly divided into a correlative module and two separate modules. MCODE clusters showed that in top 3 clusters, 13 of CMT-related genes were included in the network and 30 candidate genes were discovered which might be potentially related to CMT. The study may help to update the new understanding of the pathogenesis of CMT and expand the potential genes of CMT for further exploration.

scholarly journals P-element mutations affecting embryonic peripheral nervous system development in Drosophila melanogaster.

Genetics ◽  
1995 ◽  
Vol 139 (4) ◽  
pp. 1663-1678 ◽  
Author(s):  
A Kania ◽  
A Salzberg ◽  
M Bhat ◽  
D D'Evelyn ◽  
Y He ◽  
...  
Keyword(s):  
Nervous System ◽  
Peripheral Nervous System ◽  
Neural Development ◽  
Molecular Mechanisms ◽  
Nervous System Development ◽  
P Element ◽  
Phenotypic Characterization ◽  
Specific Marker ◽  
Element Insertion ◽  
Complementation Groups

Abstract The Drosophila embryonic peripheral nervous system (PNS) is an excellent model system to study the molecular mechanisms governing neural development. To identify genes controlling PNS development, we screened 2000 lethal P-element insertion strains. The PNS of mutant embryos was examined using the neural specific marker MAb 22C10, and 92 mutant strains were retained for further analysis. Genetic and cytological analysis of these strains shows that 42 mutations affect previously isolated genes that are known to be required for PNS development: longitudinals lacking (19), mastermind (15), numb (4), big brain (2), and spitz (2). The remaining 50 mutations were classified into 29 complementation groups and the P-element insertions were cytologically mapped. The mutants were classified in five major classes on the basis of their phenotype: gain of neurons, loss of neurons, organizational defects, pathfinding defects and morphological defects. Herein we report the preliminary phenotypic characterization of each of these complementation groups as well as the embryonic lacZ expression pattern of each P-element strain. Our analysis indicates that in most of the P-element insertion strains, the lacZ reporter gene is not expressed in the developing PNS.

scholarly journals Cell migration and axon guidance at the border between central and peripheral nervous system

Science ◽  
2019 ◽  
Vol 365 (6456) ◽  
pp. eaaw8231 ◽  
Author(s):  
Tracey A. C. S. Suter ◽  
Alexander Jaworski
Keyword(s):  
Nervous System ◽  
Cell Migration ◽  
Embryonic Development ◽  
Axon Guidance ◽  
Peripheral Nervous System ◽  
Glial Cell ◽  
Molecular Mechanisms ◽  
Control Cell ◽  
Cell Types ◽  
Open Questions

The central and peripheral nervous system (CNS and PNS, respectively) are composed of distinct neuronal and glial cell types with specialized functional properties. However, a small number of select cells traverse the CNS-PNS boundary and connect these two major subdivisions of the nervous system. This pattern of segregation and selective connectivity is established during embryonic development, when neurons and glia migrate to their destinations and axons project to their targets. Here, we provide an overview of the cellular and molecular mechanisms that control cell migration and axon guidance at the vertebrate CNS-PNS border. We highlight recent advances on how cell bodies and axons are instructed to either cross or respect this boundary, and present open questions concerning the development and plasticity of the CNS-PNS interface.

scholarly journals Imaging the Transport Dynamics of Single Alphaherpesvirus Particles in Intact Peripheral Nervous System Explants from Infected Mice

mBio ◽  
2013 ◽  
Vol 4 (3) ◽  
Author(s):  
Andrea E. Granstedt ◽  
Bingni W. Brunton ◽  
Lynn W. Enquist
Keyword(s):  
Nervous System ◽  
Salivary Gland ◽  
Peripheral Nervous System ◽  
Pseudorabies Virus ◽  
Molecular Mechanisms ◽  
Fluorescent Protein ◽  
Virus Particles ◽  
Transport Dynamics ◽  
Ganglion Neurons

ABSTRACT Alphaherpesvirus particles travel long distances in the axons of neurons using host microtubule molecular motors. The transport dynamics of individual virions in neurons have been assessed in cultured neurons, but imaging studies of single particles in tissue from infected mice have not been reported. We developed a protocol to image explanted, infected peripheral nervous system (PNS) ganglia and associated innervated tissue from mice infected with pseudorabies virus (PRV). This ex vivo preparation allowed us to visualize and track individual virions over time as they moved from the salivary gland into submandibular ganglion neurons of the PNS. We imaged and tracked hundreds of virions from multiple mice at different time points. We quantitated the transport velocity, particle stalling, duty cycle, and directionality at various times after infection. Using a PRV recombinant that expressed monomeric red fluorescent protein (mRFP)-VP26 (red capsid) and green fluorescent protein (GFP)-Us9 (green membrane protein), we corroborated that anterograde transport in axons occurs after capsids are enveloped. We addressed the question of whether replication occurs initially in the salivary gland at the site of inoculation or subsequently in the neurons of peripheral innervating ganglia. Our data indicate that significant amplification of infection occurs in the peripheral ganglia after transport from the site of infection and that these newly made particles are transported back to the salivary gland. It is likely that this reseeding of the infected gland contributes to massive invasion of the innervating PNS ganglia. We suggest that this “round-trip” infection process contributes to the characteristic peripheral neuropathy of PRV infection. IMPORTANCE Much of our understanding of molecular mechanisms of alphaherpesvirus infection and spread in neurons comes from studying cultured primary neurons. These techniques enabled significant advances in our understanding of the viral and neuronal components needed for efficient replication and directional spread between cells. However, in vitro systems cannot recapitulate the environment of innervated tissue in vivo with associated defensive properties, such as innate immunity. Therefore, in this report, we describe a system to image the progression of infection by single virus particles in tissue harvested from infected animals. We explanted intact innervated tissue from infected mice and imaged fluorescent virus particles in infected axons of the specific ganglionic neurons. Our measurements of virion transport dynamics are consistent with published in vitro results. Importantly, this system enabled us to address a fundamental biological question about the amplification of a herpesvirus infection in a peripheral nervous system circuit.

scholarly journals Acute effects of hyperglycemia on the peripheral nervous system in zebrafish (Danio rerio) following nitroreductase-mediated β-cell ablation

2019 ◽  
Vol 316 (4) ◽  
pp. R395-R405 ◽  
Author(s):  
Amanda Rocker ◽  
Julia Howell ◽  
Gabrielle Voithofer ◽  
Jessica Kennett Clark
Keyword(s):  
Nervous System ◽  
Peripheral Nervous System ◽  
Danio Rerio ◽  
Molecular Mechanisms ◽  
Motor Nerve ◽  
Control Group ◽  
Β Cell ◽  
Cell Ablation ◽  
Treated Fish ◽  
Time Point

Diabetic peripheral neuropathy (DPN) is estimated to affect 50% of diabetic patients. Although DPN is highly prevalent, molecular mechanisms remain unknown and treatment is limited to pain relief and glycemic control. We provide a novel model of acute DPN in zebrafish ( Danio rerio) larvae. Beginning 5 days postfertilization (dpf), zebrafish expressing nitroreductase in their pancreatic β-cells were treated with metronidazole (MTZ) for 48 h and checked for β-cell ablation 7 dpf. In experimental design, this was meant to serve as proof of concept that β-cell ablation and hyperglycemia are possible at this time point, but we were surprised to find changes in both sensory and motor nerve components. Compared with controls, neurod+ sensory neurons were often observed outside the dorsal root ganglia in MTZ-treated fish. Fewer motor nerves were properly ensheathed by nkx2.2a+ perineurial cells, and tight junctions were disrupted along the motor nerve in MTZ-treated fish compared with controls. Not surprisingly, the motor axons of the MTZ-treated group were defasciculated compared with the control group, myelination was attenuated, and there was a subtle difference in Schwann cell number between the MTZ-treated and control group. All structural changes occurred in the absence of behavioral changes in the larvae at this time point, suggesting that peripheral nerves are influenced by acute hyperglycemia before becoming symptomatic. Moving forward, this novel animal model of DPN will allow us to access the molecular mechanisms associated with the acute changes in the hyperglycemic peripheral nervous system, which may help direct therapeutic approaches.

Molecular mechanisms regulating myelination in the peripheral nervous system

2012 ◽  
Vol 35 (2) ◽  
pp. 123-134 ◽  
Author(s):  
Jorge A. Pereira ◽  
Frédéric Lebrun-Julien ◽  
Ueli Suter
Keyword(s):  
Nervous System ◽  
Peripheral Nervous System ◽  
Molecular Mechanisms

scholarly journals Heme Oxygenase 1 in the Nervous System: Does It Favor Neuronal Cell Survival or Induce Neurodegeneration?

2018 ◽  
Vol 19 (8) ◽  
pp. 2260 ◽  
Author(s):  
Mariapaola Nitti ◽  
Sabrina Piras ◽  
Lorenzo Brondolo ◽  
Umberto Marinari ◽  
Maria Pronzato ◽  
...  
Keyword(s):  
Nervous System ◽  
Heme Oxygenase ◽  
Molecular Mechanisms ◽  
Neuronal Damage ◽  
Neuronal Cell ◽  
System Response ◽  
Heme Oxygenase 1 ◽  
Parkinson’S Diseases ◽  
Pivotal Mechanism

Heme oxygenase 1 (HO-1) up-regulation is recognized as a pivotal mechanism of cell adaptation to stress. Under control of different transcription factors but with a prominent role played by Nrf2, HO-1 induction is crucial also in nervous system response to damage. However, several lines of evidence have highlighted that HO-1 expression is associated to neuronal damage and neurodegeneration especially in Alzheimer’s and Parkinson’s diseases. In this review, we summarize the current literature regarding the role of HO-1 in nervous system pointing out different molecular mechanisms possibly responsible for HO-1 up-regulation in nervous system homeostasis and neurodegeneration.

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