scholarly journals OBSERVATIONS ON THE FINE STRUCTURE AND CYTOCHEMISTRY OF MOUSE AND HUMAN INTERCOSTAL NEUROMUSCULAR JUNCTIONS

1961 ◽  
Vol 10 (4) ◽  
pp. 517-528 ◽  
Author(s):  
S. I. Zacks ◽  
J. M. Blumberg
Keyword(s):  
Fine Structure ◽  
Neuromuscular Junction ◽  
Neuromuscular Junctions ◽  
Surface Membrane ◽  
Basement Membranes ◽  
Intercostal Muscle ◽  
Motor End Plates ◽  
Thin Plastic ◽  
Subneural Apparatus ◽  
Amorphous Surface

The fine structure of the mouse and human intercostal muscle neuromuscular junction was studied after brief fixation in a new formol-sucrose fixative. This primary formalin fixation was followed by brief postosmication in buffered 1 per cent osmium tetroxide. Muscle blocks were embedded in methacrylate or Epon 812 epoxy resin. Marked similarities between mouse and human motor end-plates were observed. Neuromuscular junctions from both mouse and human intercostal muscle showed synaptic vesicles, primary and secondary synaptic clefts, and layered differentiation of the amorphous surface material (ASM) present on the surface of the Schwann cell plasma membrane and on the muscle surface membrane in the region of the neuromuscular junction. An attempt to stain the ASM with lead was unsuccessful. Observations on thick and thin plastic-embedded sections stained by PAS after diastase digestion showed that the ASM within the subneural apparatus is PAS positive. Alcian blue stained the endoneurium and perineurium of peripheral nerve bundles and portions of the end-plates. The similarity of the PAS-positive ASM to other basement membranes described in other sites is discussed and its possible physiologic significance within the subsynaptic apparatus is considered.

scholarly journals Glucuronylated core 1 glycans are required for precise localization of neuromuscular junctions and normal formation of basement membranes on Drosophila muscles

2018 ◽  
Vol 436 (2) ◽  
pp. 108-124 ◽  
Author(s):  
Kazuyoshi Itoh ◽  
Yoshihiro Akimoto ◽  
Shu Kondo ◽  
Tomomi Ichimiya ◽  
Kazuhiro Aoki ◽  
...  
Keyword(s):  
Neuromuscular Junctions ◽  
Basement Membranes ◽  
Precise Localization

Spontaneous potentials and fine structure of identified frog denervated neuromuscular junctions

Neuroscience ◽  
1980 ◽  
Vol 5 (1) ◽  
pp. 97-108 ◽  
Author(s):  
M.E. Kriebel ◽  
R.B. Hanna ◽  
G.D. Pappas
Keyword(s):  
Fine Structure ◽  
Neuromuscular Junctions

scholarly journals Pierson Syndrome Associated with Hypothyroidism and Septic Shock

2020 ◽  
Vol 20 (4) ◽  
pp. e385-389
Author(s):  
Areeba Ejaz ◽  
Meher B. Ali ◽  
Fatima Siddiqui ◽  
Mashal B. Ali ◽  
Ammarah Jamal
Keyword(s):  
Septic Shock ◽  
Nephrotic Syndrome ◽  
Neuromuscular Junctions ◽  
Normal Component ◽  
Congenital Nephrotic Syndrome ◽  
Psychomotor Retardation ◽  
Basement Membranes ◽  
High Dose ◽  
Converting Enzyme Inhibitors ◽  
Pierson Syndrome

Pierson syndrome is caused by mutations in the laminin β2 gene causing absent β2 laminin, which is a normal component of the basement membranes of the mature glomerulus, structures in the anterior eye and neuromuscular junctions. The mutations manifest as congenital nephrotic syndrome and microcoria which are characteristic ocular features of this disease. These mutations may also result in neurological abnormalities such as hypotonia and psychomotor retardation. We report a two-month old boy who presented to the Pediatrics Department of Dr. Ruth K. M. Pfau Civil Hospital, Karachi, Pakistan, in 2015, with the typical features of microcoria and congenital nephrotic syndrome. The hypocalcaemia, hypoproteinaemia and probable immunocompromised state consequent to nephrotic syndrome resulted in seizures, hypothyroidism and urosepsis. Despite being treated aggressively with high dose antibiotics, ionotropic support, angiotensin-converting enzyme inhibitors, thyroxine replacement and nutritional support, the infant died due to significant multiorgan disease including renal failure and septic shock. Keywords: Pierson Syndrome; Microcoria and Congenital Nephrotic Syndrome; Congenital Microcoria; Hypothyroidism; Septic Shock; Case Report; Pakistan.

scholarly journals Regulatory Function of Sympathetic Innervation on the Endo/Lysosomal Trafficking of Acetylcholine Receptor

2021 ◽  
Vol 12 ◽  
Author(s):  
Tatjana Straka ◽  
Charlotte Schröder ◽  
Andreas Roos ◽  
Laxmikanth Kollipara ◽  
Albert Sickmann ◽  
...  
Keyword(s):  
Neuromuscular Junction ◽  
Acetylcholine Receptor ◽  
Ribosomal Proteins ◽  
Neuromuscular Junctions ◽  
Sympathetic Neurons ◽  
Sympathetic Innervation ◽  
Regulatory Function ◽  
Hindlimb Muscles ◽  
Nerve Muscle

Recent studies have demonstrated that neuromuscular junctions are co-innervated by sympathetic neurons. This co-innervation has been shown to be crucial for neuromuscular junction morphology and functional maintenance. To improve our understanding of how sympathetic innervation affects nerve–muscle synapse homeostasis, we here used in vivo imaging, proteomic, biochemical, and microscopic approaches to compare normal and sympathectomized mouse hindlimb muscles. Live confocal microscopy revealed reduced fiber diameters, enhanced acetylcholine receptor turnover, and increased amounts of endo/lysosomal acetylcholine-receptor-bearing vesicles. Proteomics analysis of sympathectomized skeletal muscles showed that besides massive changes in mitochondrial, sarcomeric, and ribosomal proteins, the relative abundance of vesicular trafficking markers was affected by sympathectomy. Immunofluorescence and Western blot approaches corroborated these findings and, in addition, suggested local upregulation and enrichment of endo/lysosomal progression and autophagy markers, Rab 7 and p62, at the sarcomeric regions of muscle fibers and neuromuscular junctions. In summary, these data give novel insights into the relevance of sympathetic innervation for the homeostasis of muscle and neuromuscular junctions. They are consistent with an upregulation of endocytic and autophagic trafficking at the whole muscle level and at the neuromuscular junction.

Cell surface saccharides of Trypanosoma lewisi. I. Polycation-induced cell agglutination and fine-structure cytochemistry

1975 ◽  
Vol 19 (3) ◽  
pp. 621-644
Author(s):  
D.M. Dwyer
Keyword(s):  
Fine Structure ◽  
Cell Surface ◽  
Alcian Blue ◽  
Chondroitin Sulphate ◽  
Surface Membrane ◽  
Ruthenium Red ◽  
Surface Coat ◽  
Cell Agglutination ◽  
Trypanosoma Lewisi ◽  
Cationic Compounds

Trypanosoma lewisi bloodstream and culture forms were agglutinated differentially with low concentrations of the cationic compounds: ruthenium red, ruthenium violet, Alcian blue chloride, 1-hexadecylpyridinium chloride, lanthanum chloride, and cationized ferritin. The bloodstream form trypanosomes gave the highest agglutination levels with each of the compounds tested. Ruthenium red was the most effective inducer of cell agglutination among the several cations used. Trypsin-treated bloodstream forms were agglutinated less in the presence of ruthenium red than untreated controls. Ruthenium red-induced cell agglutination also was lowered with chondroitin sulphate and dextran sulphate, but not with alpha-D-glucose, alpha-D-mannose or with several methyl glycosides. Treatment of the bloodstream trypanosomes with alpha-amylase, dextranase, or neuraminidase had little effect on agglutination levels obtained with ruthenium red. Fine-structure cytochemical staining with ruthenium red, ruthenium violet, and Alcian blue-lanthanum nitrate was used to ascertain the presence and distribution of presumptive carbohydrates in the trypanosome cell surface. The extracellular surface coat of the bloodstream forms stained densely with each of the polycationic dyes. Trypsin treatment removed the surface coat from bloodstream trypanosomes; however, the surface membranes of the organisms were stained densely with the several dyes. Similar surface-membrane staining was obtained with the cationic compounds and the culture forms, which lack a cell surface coat. Cationized ferrin was used at the fine-structure level to visualize the negative surface charge present in the cell surface coat and external membrane of the several trypanosome stages. Results obrained from the agglutination and cytochemistry experiments indicate that complex polysaccharides are present in the surface membranes and cell surface coat of T. lewisi bloodstream forms. Similar conclusions also pertain to the surface membranes of the T. lewisi culture from trypanosomes. The carbohydrates probably represent glycopeptide and glycoprotein structural components of the surface membrane of this organism.

scholarly journals The p75NTR neurotrophin receptor is required to organize the mature neuromuscular synapse by regulating synaptic vesicle availability

2019 ◽  
Vol 7 (1) ◽  
Author(s):  
Viviana Pérez ◽  
Francisca Bermedo-Garcia ◽  
Diego Zelada ◽  
Felipe A. Court ◽  
Miguel Ángel Pérez ◽  
...  
Keyword(s):  
Neuromuscular Junction ◽  
Motor Neurons ◽  
Neuromuscular Junctions ◽  
Neuronal Damage ◽  
Neuromuscular Synapse ◽  
Force Production ◽  
Synaptic Function ◽  
Neurotrophin Receptor ◽  
Acetylcholinesterase Inhibition ◽  
Pharmacological Intervention

Abstract The coordinated movement of organisms relies on efficient nerve-muscle communication at the neuromuscular junction. After peripheral nerve injury or neurodegeneration, motor neurons and Schwann cells increase the expression of the p75NTR pan-neurotrophin receptor. Even though p75NTR targeting has emerged as a promising therapeutic strategy to delay peripheral neuronal damage progression, the effects of long-term p75NTR inhibition at the mature neuromuscular junction have not been elucidated. We performed quantitative neuroanathomical analyses of the neuromuscular junction in p75NTR null mice by laser confocal and electron microscopy, which were complemented with electromyography, locomotor tests, and pharmacological intervention studies. Mature neuromuscular synapses of p75NTR null mice show impaired postsynaptic organization and ultrastructural complexity, which correlate with altered synaptic function at the levels of nerve activity-induced muscle responses, muscle fiber structure, force production, and locomotor performance. Our results on primary myotubes and denervated muscles indicate that muscle-derived p75NTR does not play a major role on postsynaptic organization. In turn, motor axon terminals of p75NTR null mice display a strong reduction in the number of synaptic vesicles and active zones. According to the observed pre and postsynaptic defects, pharmacological acetylcholinesterase inhibition rescued nerve-dependent muscle response and force production in p75NTR null mice. Our findings revealing that p75NTR is required to organize mature neuromuscular junctions contribute to a comprehensive view of the possible effects caused by therapeutic attempts to target p75NTR.

scholarly journals Effects of Vocal Training on Thyroarytenoid Muscle Neuromuscular Junctions and Myofibers in Young and Older Rats

2020 ◽  
Author(s):  
Adrianna C Shembel ◽  
Charles Lenell ◽  
Sophia Chen ◽  
Aaron M Johnson
Keyword(s):  
Neuromuscular Junction ◽  
Muscle Fiber ◽  
Acoustic Analysis ◽  
Neuromuscular Junctions ◽  
Fiber Type ◽  
Male Rats ◽  
Brown Norway ◽  
Control Group ◽  
Vocal Training ◽  
Thyroarytenoid Muscle

Abstract The purpose of this investigation was to determine the effects of vocal training on neuromuscular junction (NMJ) morphology and muscle fiber size and composition in the thyroarytenoid muscle, the primary muscle in the vocal fold, in younger (9-month) and older (24-month) Fischer 344 × Brown Norway male rats. Over 4 or 8 weeks of vocal training, rats of both ages progressively increased their daily number of ultrasonic vocalizations (USVs) through operant conditioning and were then compared to an untrained control group. Neuromuscular junction morphology and myofiber size and composition were measured from the thyroarytenoid muscle. Acoustic analysis of USVs before and after training quantified the functional effect of training. Both 4- and 8-week training resulted in less NMJ motor endplate dispersion in the lateral portion of the thyroarytenoid muscle in rats of both ages. Vocal training and age had no significant effects on laryngeal myofiber size or type. Vocal training resulted in a greater number of USVs with longer duration and increased intensity. This study demonstrated that vocal training induces laryngeal NMJ morphology and acoustic changes. The lack of significant effects of vocal training on muscle fiber type and size suggests vocal training significantly improves neuromuscular efficiency but does not significantly influence muscle strength changes.

scholarly journals Identification of a surface membrane proton-translocating ATPase in promastigotes of the parasitic protozoan Leishmania donovani

1988 ◽  
Vol 256 (1) ◽  
pp. 13-21 ◽  
Author(s):  
D Zilberstein ◽  
D M Dwyer
Keyword(s):  
Fine Structure ◽  
Leishmania Donovani ◽  
Surface Membrane ◽  
Proton Pumping ◽  
Maximal Inhibition ◽  
Parasitic Protozoan ◽  
Immunochemical Methods ◽  
Ic50 Concentration ◽  
Proton Translocating Atpase

ATPase activities were measured in surface membranes and mitochondria isolated from promastigotes of the parasitic protozoan Leishmania donovani. The two enzymes were differentiated on the basis of pH optima, inhibitor sensitivity and by immunochemical methods. The surface-membrane (SM-) ATPase had an activity of 100 nmol/min per mg of protein, which was optimal at pH 6.5. The enzyme was Mg2+-dependent, partially inhibited by Ca2+, and unaffected by Na+ or K+. The SM-ATPase was inhibited by orthovanadate, NN'-dicyclohexylcarbodi-imide, and N-ethylmaleimide [IC50 (concentration causing half-maximal inhibition) 7.5, 25 and 520 microM respectively]; however, it was unaffected by ouabain, azide or oligomycin. The SM-ATPase demonstrated a Km of 1.05 mM and a Vmax. of 225 nmol/min per mg of protein. Moreover, fine-structure cytochemical results demonstrated that the SM-ATPase was localized to the cytoplasmic lamina of the parasite SM. A method was devised for the isolation of SM-derived vesicles. These were used to demonstrate the proton-pumping capacity of the SM-ATPase. Cumulatively, these results constitute the first demonstration of a surface-membrane proton-translocating ATPase in a parasitic protozoan.

scholarly journals In vivo recovery of muscle contraction after alpha-bungarotoxin binding.

1975 ◽  
Vol 66 (1) ◽  
pp. 209-213 ◽  
Author(s):  
H C Fertuck ◽  
W Woodward ◽  
M M Salpeter
Keyword(s):  
Fine Structure ◽  
Neuromuscular Junction ◽  
Muscle Contraction ◽  
Acetylcholine Receptors ◽  
Actinomycin D ◽  
Recovery Period ◽  
Em Autoradiography ◽  
Alpha Bungarotoxin ◽  
In Vivo Recovery

Acetylcholine receptors were inactivated in vivo at the mouse neuromuscular junction using alpha-bungarotoxin (alpha-BTX). It was found that neurally produced muscle contraction recovered within 4-8 days (halftime similar to 3 days). Actinomycin D interfered with this recovery, but did not affect normal nerve-stimulated muscle contraction. If the response was initially eliminated by [125-I]alpha-BTX and the end plates examined by EM autoradiography, no evidence of mass internalization of bound radioactivity during recovery was seen. The fine structure of the end plates and muscle was unaltered during the post-alpha-BTX recovery period.

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