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Astrow, Stephanie H.; Qiang, Huahong; Ko, Chien‐Ping

doi:10.1023/a:1006916232627

Cited by 34 publications

(3 citation statements)

References 41 publications

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“…This structure is enlarged and forms pre-synaptic boutons, which contain synaptic vesicles filled with the neurotransmitter acetylcholine (ACh). Boutons directly overlie post-synaptic invaginations of the sarcolemma called junctional folds [ 133 ], upon which high-density clusters of acetylcholine receptors (AChRs) reside. Once released into the synaptic cleft, ACh binds to AChRs, determining a local depolarization that then propagates throughout the muscle fiber.…”

Section: Age-related Alterations Of Nmj Morphology and Functionmentioning

confidence: 99%

“…These motor units differ in their physiological properties, anatomical plasticity, and susceptibility to loss of neuromuscular connectivity [ 134 - 136 ]. Specialized glial cells identified as terminal Schwann cells (tSCs) coated the nerve terminal and generate a basal lamina that merges with a muscle fiber basal lamina at the boundary of the NMJ [ 133 , 137 - 139 ]. TSCs play an important role in the plasticity, maintenance, and regeneration of NMJs.…”

Section: Age-related Alterations Of Nmj Morphology and Functionmentioning

confidence: 99%

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Semaphorins: Missing Signals in Age-dependent Alteration of Neuromuscular Junctions and Skeletal Muscle Regeneration

2023

Aging dis

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Skeletal muscle is characterized by a remarkable capacity to rearrange after physiological changes and efficiently regenerate. However, during aging, extensive injury, or pathological conditions, the complete regenerative program is severely affected, with a progressive loss of muscle mass and function, a condition known as sarcopenia. The compromised tissue repair program is attributable to the gradual depletion of stem cells and to altered regulatory signals. Defective muscle regeneration can severely affect re-innervation by motor axons, and neuromuscular junctions (NMJs) development, ultimately leading to skeletal muscle atrophy. Defects in NMJ formation and maintenance occur physiologically during aging and are responsible for the pathogenesis of several neuromuscular disorders. However, it is still largely unknown how neuromuscular connections are restored on regenerating fibers. It has been suggested that attractive and repelling signals used for axon guidance could be implicated in this process; in particular, guidance molecules called semaphorins play a key role. Semaphorins are a wide family of extracellular regulatory signals with a multifaceted role in cell-cell communication. Originally discovered as axon guidance factors, they have been implicated in cancer progression, embryonal organogenesis, skeletal muscle innervation, and other physiological and developmental functions in different tissues. In particular, in skeletal muscle, specific semaphorin molecules are involved in the restoration and remodeling of the nerve-muscle connections, thus emphasizing their plausible role to ensure the success of muscle regeneration. This review article aims to discuss the impact of aging on skeletal muscle regeneration and NMJs remodeling and will highlight the most recent insights about the role of semaphorins in this context.

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Section: Age-related Alterations Of Nmj Morphology and Functionmentioning

confidence: 99%

Section: Age-related Alterations Of Nmj Morphology and Functionmentioning

confidence: 99%

Semaphorins: Missing Signals in Age-dependent Alteration of Neuromuscular Junctions and Skeletal Muscle Regeneration

2023

Aging dis

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“…Boutons directly overlie post-synaptic invaginations of the sarcolemma called junctional folds [ 1 ], upon which high-density clusters of acetylcholine receptors (AChRs) reside. Interdigitated between post-junctional folds are the perisynaptic Schwann cells (PSCs), which are glial regulators of NMJ structure and function [ 2 ]. When released into the synaptic cleft, ACh binds to AChRs, causing an endplate potential (EPP), a local depolarization that then propagates throughout the muscle fiber as a conducted action potential.…”

Section: Introductionmentioning

confidence: 99%

The Neuromuscular Junction: Roles in Aging and Neuromuscular Disease

Iyer

Shah

Lovering

2021

IJMS

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The neuromuscular junction (NMJ) is a specialized synapse that bridges the motor neuron and the skeletal muscle fiber and is crucial for conversion of electrical impulses originating in the motor neuron to action potentials in the muscle fiber. The consideration of contributing factors to skeletal muscle injury, muscular dystrophy and sarcopenia cannot be restricted only to processes intrinsic to the muscle, as data show that these conditions incur denervation-like findings, such as fragmented NMJ morphology and corresponding functional changes in neuromuscular transmission. Primary defects in the NMJ also influence functional loss in motor neuron disease, congenital myasthenic syndromes and myasthenia gravis, resulting in skeletal muscle weakness and heightened fatigue. Such findings underscore the role that the NMJ plays in neuromuscular performance. Regardless of cause or effect, functional denervation is now an accepted consequence of sarcopenia and muscle disease. In this short review, we provide an overview of the pathologic etiology, symptoms, and therapeutic strategies related to the NMJ. In particular, we examine the role of the NMJ as a disease modifier and a potential therapeutic target in neuromuscular injury and disease.

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Reciprocal interactions between perisynaptic Schwann cells and regenerating nerve terminals at the frog neuromuscular junction

Koirala

Qiang

2000

J. Neurobiol.

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The perisynaptic Schwann cell (PSC) has gained recent attention with respect to its roles in synaptic function, remodeling, and regeneration at the vertebrate neuromuscular junction (NMJ). Here we test the hypothesis that, following nerve injury, processes extended by PSCs guide regenerating nerve terminals (NTs) in vivo, and that the extension of sprouts by PSCs is triggered by the arrival of regenerating NTs. Frog NMJs were double‐stained with a fluorescent dye, FM4‐64, for NTs, and fluorescein isothiocyanate (FITC)‐tagged peanut agglutinin (PNA) for PSCs. Identified NMJs were imaged in vivo repeatedly for several months after nerve injury. PSCs sprouted profusely beginning 3–4 weeks after nerve transection and, as reinnervation progressed, regenerating NTs closely followed the preceding PSC sprouts, which could extend tens to hundreds of microns beyond the original synaptic site. The pattern of reinnervation was dictated by PSC sprouts, which could form novel routes joining neighboring junctions or develop into new myelinated axonal pathways. In contrast to mammals, profuse PSC sprouting in frog muscles was not seen in response to axotomy alone, and did not occur at chronically denervated NMJs. Instead, sprouting coincided with the arrival of regenerating NTs. Immunofluorescent staining revealed that in muscle undergoing reinnervation 4 weeks after axotomy, 91% of NMJs bore PSC sprouts, compared to only 6% of NMJs in muscle that was chronically denervated for 4 weeks. These results suggest that reciprocal interactions between regenerating NTs and PSCs govern the process of reinnervation at frog NMJs: regenerating NTs induce PSCs to sprout, and PSC sprouts, in turn, lead and guide the elaboration of NTs. © 2000 John Wiley & Sons, Inc. J Neurobiol 44: 343–360, 2000

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Cited by 34 publications

References 41 publications

Semaphorins: Missing Signals in Age-dependent Alteration of Neuromuscular Junctions and Skeletal Muscle Regeneration

Semaphorins: Missing Signals in Age-dependent Alteration of Neuromuscular Junctions and Skeletal Muscle Regeneration

The Neuromuscular Junction: Roles in Aging and Neuromuscular Disease

Reciprocal interactions between perisynaptic Schwann cells and regenerating nerve terminals at the frog neuromuscular junction

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