scholarly journals Perisynaptic Schwann Cells at the Neuromuscular Synapse: Adaptable, Multitasking Glial Cells

2015 ◽  
Vol 7 (10) ◽  
pp. a020503 ◽  
Author(s):  
Chien-Ping Ko ◽  
Richard Robitaille
Keyword(s):  
Schwann Cells ◽  
Glial Cells ◽  
Neuromuscular Synapse ◽  
Perisynaptic Schwann Cells

scholarly journals Activity-induced Ca2+ signaling in perisynaptic Schwann cells of the early postnatal mouse is mediated by P2Y1 receptors and regulates muscle fatigue

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Dante J Heredia ◽  
Cheng-Yuan Feng ◽  
Grant W Hennig ◽  
Robert B Renden ◽  
Thomas W Gould
Keyword(s):  
Muscle Fatigue ◽  
Schwann Cells ◽  
Glial Cells ◽  
Nerve Stimulation ◽  
Neural Activity ◽  
Purinergic Receptor ◽  
Cytosolic Calcium ◽  
High Potassium ◽  
Presynaptic Function ◽  
Perisynaptic Schwann Cells

Perisynaptic glial cells respond to neural activity by increasing cytosolic calcium, but the significance of this pathway is unclear. Terminal/perisynaptic Schwann cells (TPSCs) are a perisynaptic glial cell at the neuromuscular junction that respond to nerve-derived substances such as acetylcholine and purines. Here, we provide genetic evidence that activity-induced calcium accumulation in neonatal TPSCs is mediated exclusively by one subtype of metabotropic purinergic receptor. In P2ry1 mutant mice lacking these responses, postsynaptic, rather than presynaptic, function was altered in response to nerve stimulation. This impairment was correlated with a greater susceptibility to activity-induced muscle fatigue. Interestingly, fatigue in P2ry1 mutants was more greatly exacerbated by exposure to high potassium than in control mice. High potassium itself increased cytosolic levels of calcium in TPSCs, a response which was also reduced P2ry1 mutants. These results suggest that activity-induced calcium responses in TPSCs regulate postsynaptic function and muscle fatigue by regulating perisynaptic potassium.

scholarly journals Murine Esophagus Expresses Glial-Derived Central Nervous System Antigens

2021 ◽  
Vol 22 (6) ◽  
pp. 3233
Author(s):  
Christopher Kapitza ◽  
Rittika Chunder ◽  
Anja Scheller ◽  
Katherine S. Given ◽  
Wendy B. Macklin ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Schwann Cells ◽  
Glial Cells ◽  
Proteolipid Protein ◽  
Pcr Analysis ◽  
Specific Expression ◽  
Enteric Glial Cells ◽  
Cell Type Specific Expression ◽  
Long Time

Multiple sclerosis (MS) has been considered to specifically affect the central nervous system (CNS) for a long time. As autonomic dysfunction including dysphagia can occur as accompanying phenomena in patients, the enteric nervous system has been attracting increasing attention over the past years. The aim of this study was to identify glial and myelin markers as potential target structures for autoimmune processes in the esophagus. RT-PCR analysis revealed glial fibrillary acidic protein (GFAP), proteolipid protein (PLP), and myelin basic protein (MBP) expression, but an absence of myelin oligodendrocyte glycoprotein (MOG) in the murine esophagus. Selected immunohistochemistry for GFAP, PLP, and MBP including transgenic mice with cell-type specific expression of PLP and GFAP supported these results by detection of (1) GFAP, PLP, and MBP in Schwann cells in skeletal muscle and esophagus; (2) GFAP, PLP, but no MBP in perisynaptic Schwann cells of skeletal and esophageal motor endplates; (3) GFAP and PLP, but no MBP in glial cells surrounding esophageal myenteric neurons; and (4) PLP, but no GFAP and MBP in enteric glial cells forming a network in the esophagus. Our results pave the way for further investigations regarding the involvement of esophageal glial cells in the pathogenesis of dysphagia in MS.

scholarly journals Terminal Schwann Cells Participate in Neuromuscular Synapse Remodeling during Reinnervation following Nerve Injury

2014 ◽  
Vol 34 (18) ◽  
pp. 6323-6333 ◽  
Author(s):  
H. Kang ◽  
L. Tian ◽  
M. Mikesh ◽  
J. W. Lichtman ◽  
W. J. Thompson
Keyword(s):  
Schwann Cells ◽  
Nerve Injury ◽  
Neuromuscular Synapse ◽  
Terminal Schwann Cells

scholarly journals SV40T reprograms Schwann cells into stem-like cells that can re-differentiate into terminal nerve cells

2021 ◽  
Author(s):  
Rui-fang Li ◽  
Guo-xin Nan ◽  
Dan Wang ◽  
Chang Gao ◽  
Juan Yang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Neural Stem Cells ◽  
Neural Crest ◽  
Schwann Cells ◽  
Early Development ◽  
Glial Cells ◽  
Embryonic Stem ◽  
Specific Effect ◽  
Neural Crest Cells

Background: The specific effect of SV40T on neurocytes has been rarely investigated by the researchers. We transfected Schwann cells (SCs) that did not have differentiation ability with MPH 86 plasmid containing SV40T in order to explore the effects of SV40T on Schwann cells.Methods: SCs were transfected with MPH 86 plasmid carrying the SV40T gene and cultured in different media, as well as co-cultured with neural stem cells (NSCs). In our study, SCs overexpressing SV40T were defined as SV40T-SCs. The proliferation of these cells was detected by WST-1, and the expression of different biomarkers was analyzed by qPCR and immunohistochemistry. Results: SV40T induced the characteristics of NSCs, such as the ability to grow in suspension, form spheroid colonies and proliferate rapidly, in the SCs, which were reversed by knocking out SV40T by the Flip-adenovirus. In addition, SV40T upregulated the expressions of neural crest-associated markers Nestin, Pax3 and Slug, and down-regulated S100b as well as the markers of mature SCs MBP, GFAP and Olig1/2. These cells also expressed NSC markers like Nestin, Sox2, CD133 and SSEA-1, as well as early development markers of embryonic stem cells (ESCs) like BMP4, c-Myc, OCT4 and Gbx2. Co-culturing with NSCs induced differentiation of the SV40T-SCs into neuronal and glial cells. Conclusions: SV40T reprograms Schwann cells to stem-like cells at the stage of neural crest cells (NCCs) that can differentiate to neurocytes.

Perspectives in Pain Research 2014: Neuroinflammation and glial cell activation: The cause of transition from acute to chronic pain?

2015 ◽  
Vol 6 (1) ◽  
pp. 3-6 ◽  
Author(s):  
Brian E. Cairns ◽  
Lars Arendt-Nielsen ◽  
Paola Sacerdote
Keyword(s):  
Spinal Cord ◽  
Chronic Pain ◽  
Dorsal Root Ganglion ◽  
Glial Cell ◽  
Schwann Cells ◽  
Glial Cells ◽  
Proinflammatory Cytokines ◽  
Immune Cells ◽  
Dorsal Root ◽  
Satellite Glial Cells

AbstractBackgroundIt is unknown why an acute pain condition under various circumstances can transition into a chronic pain condition.There has been a shift towards neuroinflammation and hence glial cell activations specifically in the dorsal root ganglion and spinal cord as a mechanism possibly driving the transition to chronic pain. This has led to a focus on non-neuronal cells in the peripheral and central nervous system. Besides infiltrating macrophages, Schwann cells and satellite glial cells release cytokines and therefore important mechanisms in the maintenance of pain. Activated Schwann cells, satellite glial cells, microglia, and astrocytes may contribute to pain sensitivity by releasing cytokines leading to altered neuronal function in the direction of sensitisation.Aims of this perspective paper1) Highlight the complex but important recent achievement in the area of neuroinflammation and pain at spinal cord level and in the dorsal root ganglion.2) Encourage further research which hopefully may provide better understanding of new key elements driving the transition from acute to chronic pain.Recent results in the area of neuroinflammation and painFollowing a sciatic nerve injury, local macrophages, and Schwann cells trigger an immune response immediately followed by recruitment of blood-derived immune cells. Schwann cells, active resident, and infiltrating macrophages release proinflammatory cytokines. Proinflammatory cytokines contribute to axonal damage and also stimulate spontaneous nociceptor activity. This results in activation of satellite glial cells leading to an immune response in the dorsal root ganglia driven by macrophages, lymphocytes and satellite cells. The anterograde signalling progresses centrally to activate spinal microglia with possible up regulation of glial-derived proinflammatory/pronociceptive mediators.An important aspect is extrasegmental spreading sensitisation where bilateral elevations in TNF-α, IL-6, and IL-10 are found in dorsal root ganglion in neuropathic models. Similarly in inflammatory pain models, bilateral up regulation occurs for TNF-α, IL-1 β, and p38 MAPK. Bilateral alterations in cytokine levels in the DRG and spinal cord may underlie the spread of pain to the uninjured side.An important aspect is how the opioids may interact with immune cells as opioid receptors are expressed by peripheral immune cells and thus can induce immune signaling changes. Furthermore, opioids may stimulate microglia cells to produce proinflammatory cytokines such as IL-1.ConclusionsThe present perspective paper indicates that neuroinflammation and the associated release of pro-inflammatory cytokines in dorsal root ganglion and at the spinal cord contribute to the transition from acute to chronic pain. Neuroinflammatory changes have not only been identified in the spinal cord and brainstem, but more recently, in the sensory ganglia and in the nerves as well. The glial cell activation may be responsible for contralateral spreading and possible widespread sensitisation.ImplicationsCommunication between glia and neurons is proposed to be a critical component of neuroinflammatory changes that may lead to chronic pain. Sensory ganglia neurons are surrounded by satellite glial cells but how communication between the cells contributes to altered pain sensitivity is still unknown. Better understanding may lead to new possibilities for (1) preventing development of chronic pain and (2) better pain management.

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