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Neuromuscular junction

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https://www.readbyqxmd.com/read/29455227/the-clinical-features-of-patients-concurrent-with-guillain-barre-syndrome-and-myasthenia-gravis
#1
Junliang Yuan, Juan Zhang, Bingwei Zhang, Wenli Hu
OBJECTIVE: To evaluate all the coincidence cases of Guillain-Barre syndrome (GBS) and myasthenia gravis (MG). METHODS: We performed web-based research of the overlapping incidence of GBS and MG in studies occurring from 1982 to 2016 and restricted to the English language. RESULTS: Among 15 cases, an elevated CSF protein level without pleocytosis was found in 10 cases (66.7%); reduced nerve conduction was found in 13 cases (86.6%); a positive repetitive nerve stimulation test occurred in 11 cases (73...
January 2018: Neurosciences: the Official Journal of the Pan Arab Union of Neurological Sciences
https://www.readbyqxmd.com/read/29453960/synaptic-dysfunction-and-altered-excitability-in-c9orf72-als-ftd
#2
Alexander Starr, Rita Sattler
Amyotrophic lateral sclerosis (ALS) is characterized by a progressive degeneration of upper and lower motor neurons, resulting in fatal paralysis due to denervation of the muscle. Due to genetic, pathological and symptomatic overlap, ALS is now considered a spectrum disease together with frontotemporal dementia (FTD), the second most common cause of dementia in individuals under the age of 65. Interestingly, in both diseases, there is a large prevalence of RNA binding proteins (RBPs) that are mutated and considered disease-causing, or whose dysfunction contribute to disease pathogenesis...
February 14, 2018: Brain Research
https://www.readbyqxmd.com/read/29450865/erratum-to-super-resolution-single-molecule-fish-at-the-drosophila-neuromuscular-junction
#3
Joshua S Titlow, Lu Yang, Richard M Parton, Ana Palanca, Ilan Davis
No abstract text is available yet for this article.
2018: Methods in Molecular Biology
https://www.readbyqxmd.com/read/29440993/increasing-agrin-function-antagonizes-muscle-atrophy-and-motor-impairment-in-spinal-muscular-atrophy
#4
Marina Boido, Elena De Amicis, Valeria Valsecchi, Marco Trevisan, Ugo Ala, Markus A Ruegg, Stefan Hettwer, Alessandro Vercelli
Spinal muscular atrophy (SMA) is a pediatric genetic disease, characterized by motor neuron (MN) death, leading to progressive muscle weakness, respiratory failure, and, in the most severe cases, to death. Abnormalities at the neuromuscular junction (NMJ) have been reported in SMA, including neurofilament (NF) accumulation at presynaptic terminals, immature and smaller than normal endplates, reduced transmitter release, and, finally, muscle denervation. Here we have studied the role of agrin in SMAΔ7 mice, the experimental model of SMAII...
2018: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/29436006/endogenous-purines-modulate-k-evoked-ach-secretion-at-the-mouse-neuromuscular-junction
#5
Juan F Guarracino, Alejandro R Cinalli, Mariela I Veggetti, Adriana S Losavio
At the mouse neuromuscular junction, adenosine triphosphate (ATP) is co-released with the neurotransmitter acetylcholine (ACh), and once in the synaptic cleft, it is hydrolyzed to adenosine. Both ATP/adenosine diphosphate (ADP) and adenosine modulate ACh secretion by activating presynaptic P2Y13 and A1 , A2A , and A3 receptors, respectively. To elucidate the action of endogenous purines on K+ -dependent ACh release, we studied the effect of purinergic receptor antagonists on miniature end-plate potential (MEPP) frequency in phrenic diaphragm preparations...
February 13, 2018: Journal of Neuroscience Research
https://www.readbyqxmd.com/read/29434186/preconditioning-induced-by-sub-toxic-dose-of-the-neurotoxin-l-bmaa-delays-als-progression-in-mice-and-prevents-na-ca2-exchanger-3-downregulation
#6
Serenella Anzilotti, Paola Brancaccio, Giuseppe Simeone, Valeria Valsecchi, Antonio Vinciguerra, Agnese Secondo, Tiziana Petrozziello, Natascia Guida, Rossana Sirabella, Ornella Cuomo, Pasquale Cepparulo, Andrè Herchuelz, Salvatore Amoroso, Gianfranco Di Renzo, Lucio Annunziato, Giuseppe Pignataro
Preconditioning (PC) is a phenomenon wherein a mild insult induces resistance to a later, severe injury. Although PC has been extensively studied in several neurological disorders, no studies have been performed in amyotrophic lateral sclerosis (ALS). Here we hypothesize that a sub-toxic acute exposure to the cycad neurotoxin beta-methylamino-L-alanine (L-BMAA) is able to delay ALS progression in SOD1 G93A mice and that NCX3, a membrane transporter able to handle the deregulation of ionic homeostasis occurring during ALS, takes part to this neuroprotective effect...
February 12, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29432799/mitochondrial-protein-s-nitrosation-protects-against-ischemia-reperfusion-induced-denervation-at-neuromuscular-junction-in-skeletal-muscle
#7
Rebecca J Wilson, Joshua C Drake, Di Cui, Bevan M Lewellen, Carleigh C Fisher, Mei Zhang, David F Kashatus, Lisa A Palmer, Michael P Murphy, Zhen Yan
Deterioration of neuromuscular junction (NMJ) integrity and function is causal to muscle atrophy and frailty, ultimately hindering quality of life and increasing the risk of death. In particular, NMJ is vulnerable to ischemia reperfusion (IR) injury when blood flow is restricted followed by restoration. However, little is known about the underlying mechanism(s) and hence the lack of effective interventions. New evidence suggests that mitochondrial oxidative stress plays a causal role in IR injury, which can be precluded by enhancing mitochondrial protein S-nitrosation (SNO)...
February 9, 2018: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/29432681/pharming-for-genes-in-neurotransmission-combining-chemical-and-genetic-approaches-in-c-elegans
#8
Stephen M Blazie, Yishi Jin
Synaptic transmission is central to nervous system function. Chemical and genetic screens are valuable approaches to probe synaptic mechanisms in living animals. The nematode C. elegans is a prime system to apply these methods to discover genes and dissect the cellular pathways underlying neurotransmission. Here, we review key approaches to understand neurotransmission and the action of psychiatric drugs in C. elegans, starting with early studies on cholinergic excitatory signaling at the neuromuscular junction and moving into mechanisms mediated by biogenic amine and psychiatric drugs...
February 12, 2018: ACS Chemical Neuroscience
https://www.readbyqxmd.com/read/29431032/decellularized-muscle-supports-new-muscle-fibers-and-improves-function-following-volumetric-injury
#9
Michael James McClure, David Josh Cohen, Allison N Ramey, Caroline B Bivens, Satya Mallu, Jonathan E Isaacs, Emily Imming, Yen-Chen Huang, MoonHae Sunwoo, Zvi Schwartz, Barbara Boyan
Current strategies to treat volumetric muscle loss use primarily pedicle or free muscle transfers, but these grafts fail to adequately regenerate functional tissue. Decellularized soft tissue grafts possess physical and chemical cues to promote muscle regeneration, suggesting their potential for use in large muscle defects. In this study, we developed a decellularized muscle matrix (DMM) graft using rat gastrocnemius. Anisotropy and chemical components of the extracellular matrix were retained, including laminin, fibronectin, and collagen...
February 12, 2018: Tissue Engineering. Part A
https://www.readbyqxmd.com/read/29427317/overexpression-of-pgc-1%C3%AE-in-aging-muscle-enhances-a-subset-of-young-like-molecular-patterns
#10
Sofia Garcia, Nadee Nissanka, Edson A Mareco, Susana Rossi, Susana Peralta, Francisca Diaz, Richard L Rotundo, Robson F Carvalho, Carlos T Moraes
PGC-1α is a transcriptional co-activator known as the master regulator of mitochondrial biogenesis. Its control of metabolism has been suggested to exert critical influence in the aging process. We have aged mice overexpressing PGC-1α in skeletal muscle to determine whether the transcriptional changes reflected a pattern of expression observed in younger muscle. Analyses of muscle proteins showed that Pax7 and several autophagy markers were increased. In general, the steady-state levels of several muscle proteins resembled that of muscle from young mice...
February 10, 2018: Aging Cell
https://www.readbyqxmd.com/read/29421431/introducing-autoimmunity-at-the-synapse-by-a-novel-animal-model-of-experimental-autoimmune-myasthenia-gravis
#11
REVIEW
Jianwen Wang, Yatao Xiao, Kejing Zhang, Benyan Luo, Chengyong Shen
The neuromuscular junction (NMJ) is a peripheral synapse between motor neurons and skeletal muscle fibers that controls muscle contraction. The NMJ is the target of various disorders including myasthenia gravis (MG), an autoimmune disease in which auto-antibodies (auto-Abs) attack the synapse, and thus cause muscle weakness in patients. There are multiple auto-Abs in the MG patient sera, but not all the Abs are proven to be pathogenic, which increases the difficulties in clinical diagnoses and treatments. To establish the causative roles of auto-Abs in MG pathogenesis, the experimental autoimmune MG (EAMG) induced by the active immunization of auto-antigens (auto-Ags) or the passive transfer of auto-Abs is required...
February 5, 2018: Neuroscience
https://www.readbyqxmd.com/read/29415512/linking-extracellular-matrix-agrin-to-the-hippo-pathway-in-liver-cancer-and-beyond
#12
REVIEW
Sayan Chakraborty, Wanjin Hong
In addition to the structural and scaffolding role, the extracellular matrix (ECM) is emerging as a hub for biomechanical signal transduction that is frequently relayed to intracellular sensors to regulate diverse cellular processes. At a macroscopic scale, matrix rigidity confers long-ranging effects contributing towards tissue fibrosis and cancer. The transcriptional co-activators YAP/TAZ, better known as the converging effectors of the Hippo pathway, are widely recognized for their new role as nuclear mechanosensors during organ homeostasis and cancer...
February 6, 2018: Cancers
https://www.readbyqxmd.com/read/29414833/increased-proportion-of-tc17-and-th17-cells-and-their-significant-reduction-after-thymectomy-may-be-related-to-disease-progression-in-myasthenia-gravis
#13
Mina Hosseini, Behrouz Robat-Jazi, Vahid Shaygannejad, Shahriar Naffisi, Omid Mirmossayeb, Abbas Rezaei, Marjan Mansourian, Nafiseh Esmaeil
OBJECTIVE: Myasthenia gravis (MG) is an autoimmune disease mediated by autoantibodies against the neuromuscular junction. The thymus has an important role in the pathogenesis of MG because most patients have thymic pathology, and thymectomy (TE) can reduce the severity of the disease. METHODS: In this study, the frequency of Th17 and Tc17 cells was studied in 12 MG patients (pre-TE and 6 months post-TE) and in 12 healthy controls (HC). RESULTS: The frequency of Tc17 cells in the pre-TE patients was significantly higher than in the HC (p < 0...
February 8, 2018: Neuroimmunomodulation
https://www.readbyqxmd.com/read/29411505/transcriptomics-of-aged-drosophila-motor-neurons-reveals-a-matrix-metalloproteinase-that-impairs-motor-function
#14
Jorge Azpurua, Rebekah E Mahoney, Benjamin A Eaton
The neuromuscular junction (NMJ) is responsible for transforming nervous system signals into motor behavior and locomotion. In the fruit fly Drosophila melanogaster, an age-dependent decline in motor function occurs, analogous to the decline experienced in mice, humans, and other mammals. The molecular and cellular underpinnings of this decline are still poorly understood. By specifically profiling the transcriptome of Drosophila motor neurons across age using custom microarrays, we found that the expression of the matrix metalloproteinase 1 (dMMP1) gene reproducibly increased in motor neurons in an age-dependent manner...
February 7, 2018: Aging Cell
https://www.readbyqxmd.com/read/29410956/effect-of-hyperglycemia-on-purinergic-and-nitrergic-inhibitory-neuromuscular-transmission-in-the-antrum-of-the-stomach-implications-for-fast-gastric-emptying
#15
Xue-Dao He, Yan-Mei Guo, Raj K Goyal
Background: Hyperglycemia has been reported to enhance vagovagal reflex that causes the release of inhibitory neurotransmitter, nitric oxide (NO), at the neuromuscular junction in the antrum to relax the antrum and slow gastric emptying by stimulating glucose-sensitive afferent neurons. However, hyperglycemia has also been reported to cause fast gastric emptying that may be due to suppression of the inhibitory motor neurons. Aims: The purpose of the present study was to investigate changes in inhibitory neuromuscular transmission in the gastric antrum due to hyperglycemia...
2018: Frontiers in Medicine
https://www.readbyqxmd.com/read/29410613/neuronal-lipid-metabolism-multiple-pathways-driving-functional-outcomes-in-health-and-disease
#16
REVIEW
Timothy J Tracey, Frederik J Steyn, Ernst J Wolvetang, Shyuan T Ngo
Lipids are a fundamental class of organic molecules implicated in a wide range of biological processes related to their structural diversity, and based on this can be broadly classified into five categories; fatty acids, triacylglycerols (TAGs), phospholipids, sterol lipids and sphingolipids. Different lipid classes play major roles in neuronal cell populations; they can be used as energy substrates, act as building blocks for cellular structural machinery, serve as bioactive molecules, or a combination of each...
2018: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/29409912/crush-injury-to-motor-nerves-in-the-g93a-transgenic-mouse-model-of-amyotrophic-lateral-sclerosis-promotes-muscle-reinnervation-and-survival-of-functionally-intact-nerve-muscle-contacts
#17
P S Sharp, N Tyreman, K Jones, T Gordon
Selective survival of small motor nerve fibers and their neuromuscular contacts in the SOD1G93A transgenic mouse model of amyotrophic lateral sclerosis (ALS) suggests that smaller regenerated nerve fibers are more able to sustain reformed nerve-muscle connections as functionally intact motor units (MUs). The sciatic nerve was crushed unilaterally in SOD1G93A transgenic mice at 40 days of age and contractile forces of reinnervated muscles and their MUs were recorded at 90 days in order to determine the capacities of the nerves to regenerate and to form and retain functional neuromuscular connections...
January 30, 2018: Neurobiology of Disease
https://www.readbyqxmd.com/read/29408692/proteomic-analysis-of-the-sarcolemma-enriched-fraction-from-dystrophic-mdx-4cv-skeletal-muscle
#18
Sandra Murphy, Margit Zweyer, Michael Henry, Paula Meleady, Rustam R Mundegar, Dieter Swandulla, Kay Ohlendieck
The highly progressive neuromuscular disorder dystrophinopathy is triggered by primary abnormalities in the Dmd gene, which causes cytoskeletal instability and loss of sarcolemmal integrity. Comparative organellar proteomics was employed to identify sarcolemma-associated proteins with an altered concentration in dystrophic muscle tissue from the mdx-4cv mouse model of dystrophinopathy. A lectin agglutination method was used to prepare a sarcolemma-enriched fraction and resulted in the identification of 190 significantly changed protein species...
February 1, 2018: Journal of Proteomics
https://www.readbyqxmd.com/read/29408646/utrophin-up-regulation-by-artificial-transcription-factors-induces-muscle-rescue-and-impacts-the-neuromuscular-junction-in-mdx-mice
#19
Cinzia Pisani, Georgios Strimpakos, Francesca Gabanella, Maria Grazia Di Certo, Annalisa Onori, Cinzia Severini, Siro Luvisetto, Stefano Farioli-Vecchioli, Irene Carrozzo, Antonio Esposito, Tamara Canu, Elisabetta Mattei, Nicoletta Corbi, Claudio Passananti
Up-regulation of the dystrophin-related gene utrophin represents a promising therapeutic strategy for the treatment of Duchenne Muscular Dystrophy (DMD). In order to re-program the utrophin expression level in muscle, we engineered artificial zinc finger transcription factors (ZF-ATFs) that target the utrophin "A" promoter. We have previously shown that the ZF-ATF "Jazz", either by transgenic manipulation or by systemic adeno-associated viral delivery, induces significant rescue of muscle function in dystrophic "mdx" mice...
January 30, 2018: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/29405353/congenital-myasthenic-syndromes-with-acetylcholinesterase-deficiency-the-pathophysiological-mechanisms
#20
REVIEW
Claire Legay
The neuromuscular junction (NMJ) is a cholinergic synapse in vertebrates. This synapse connects motoneurons to muscles and is responsible for muscle contraction, a physiological process that is essential for survival. A key factor for the normal functioning of this synapse is the regulation of acetylcholine (ACh) levels in the synaptic cleft. This is ensured by acetylcholinesterase (AChE), which degrades ACh. A number of mutations in synaptic genes expressed in motoneurons or muscle cells have been identified and are causative for a class of neuromuscular diseases called congenital myasthenic syndromes (CMSs)...
February 2018: Annals of the New York Academy of Sciences
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