Aminergic and peptidergic modulation of motor function at an identified neuromuscular junction in Helisoma

1989 ◽  
Vol 142 (1) ◽  
pp. 225-243
Author(s):  
M. J. Zoran ◽  
P. G. Haydon ◽  
P. J. Matthews
Keyword(s):  
Muscle Fibre ◽  
Muscle Cells ◽  
Muscle Contractions ◽  
Interactive Effects ◽  
Muscle Fibres ◽  
Buccal Ganglion ◽  
Motor Pathway ◽  
Peripheral Muscle ◽  
Electrophysiological Studies

Electrophysiological studies suggest that motoneurone B19 in the buccal ganglia of Helisoma makes monosynaptic, cholinergic connections with the supralateral radular tensor (SLT) muscle of the buccal mass. Serotonin (5-HT) and small cardioactive peptide B (SCPB) were found to have peripheral modulatory effects on this motor pathway that are consistent with their previously described central facilitatory effects. Both neurotransmitters, when applied exogenously (10(−6) mol l-1) to isolated buccal ganglion-buccal muscle preparations, potentiated the magnitude of motoneurone B19-evoked muscle contractions (6.3 and 2.7 times, respectively) without affecting excitatory junctional potential (EJP) amplitudes. When applied to single dissociated SLT muscle fibres in cell culture, these modulators had similar effects on acetylcholine (ACh)-evoked muscle fibre shortening, demonstrating that these neuromodulators exert direct actions on the muscle cells. The cardioactive peptide FMRFamide (10(−6) mol l-1), although slightly potentiating muscle contractions in reduced neuromuscular preparations, significantly decreased both ACh-evoked muscle fibre shortening and depolarizing potentials in cultured SLT muscle cells. The differential effects of FMRFamide may, in part, be due to the elimination of interactive effects between multiple neurotransmitters that might exist in semi-intact preparations and in vivo. These results demonstrate that 5-HT, SCPB and FMRFamide in Helisoma can directly modulate the peripheral muscle targets of buccal motoneurones involved in the generation of cyclical feeding behaviour.

Differential inflammatory modulation of canine ileal longitudinal and circular muscle cells

1999 ◽  
Vol 277 (2) ◽  
pp. G341-G350 ◽  
Author(s):  
Xuan-Zheng Shi ◽  
Sushil K. Sarna
Keyword(s):  
Receptor Antagonist ◽  
Muscarinic Receptor ◽  
Longitudinal Muscle ◽  
Circular Muscle ◽  
Muscle Cells ◽  
Muscle Contractions ◽  
Receptor Subtypes ◽  
Relative Role

The aim of this study was to identify the subtypes of muscarinic receptors that mediate in vivo and in vitro canine ileal longitudinal muscle contractions and whether their role is modulated by inflammation. Previous studies have reported that circular muscle contractions are suppressed in ileal inflammation induced by mucosal exposure to ethanol and acetic acid. We found that inflammation had no significant effect on in vivo and in vitro spontaneous or muscarinic receptor-mediated contractions of the longitudinal muscle. The longitudinal muscle contractions were mediated primarily by the M3 receptor subtype. However, the IC50 of the M2 receptor antagonist methoctramine was only 10 times greater than that of the M3 receptor antagonist 4-DAMP in the longitudinal muscle, whereas it was 224 times greater in the circular muscle. M2receptor-coupled decrease of intracellular cAMP occurred in the longitudinal but not in the circular muscle from the normal ileum. Inflammation did not alter this coupling in the longitudinal muscle but established it in the circular muscle. In conclusion, M2 receptors may play a greater role in the mediation of longitudinal muscle contractions than circular muscle contractions. Inflammation does not alter the contractility or the relative role of muscarinic receptor subtypes in longitudinal muscle cells. However, it modulates the M2 receptor coupling to adenylate cyclase in the circular muscle.

Embryonic growth and innervation of rat skeletal muscles. - III. Neural regulation of junctional and extra-junctional acetylcholine receptor clusters

1981 ◽  
Vol 293 (1065) ◽  
pp. 287-314 ◽  
Keyword(s):  
Muscle Fibre ◽  
Nerve Terminal ◽  
Time Course ◽  
Muscle Development ◽  
Muscle Cells ◽  
Diaphragm Muscle ◽  
Muscle Fibres ◽  
The Mean ◽  
Receptor Clusters ◽  
Ach Receptors

The number and distribution of acetylcholine (ACh) receptors on muscle cells was studied during development of normal, paralysed and aneural embryonic rat diaphragm muscles. (i) ACh receptors initially are dispersed over the surface of rat embryo myotubes. At day 15| of gestation junctional receptor clusters (‘J-clusters’) form in a well ordered band across the midline of the diaphragm muscle; these also form in denervated and paralysed muscles. At about day 18 of gestation additional ‘EJ-clusters’ develop to either side of the midpoint of treated muscles. (ii) If a nerve terminal is present, J-clusters increase in length with time. The time course of generation of new endplates calculated from frequency distributions of J-cluster lengths accurately predicts the muscle growth curve established from muscle fibre counts. (iii) The mean length of J-clusters in paralysed muscles was greater than in controls, due to small new-formed clusters failing to appear. In muscles allowed to recover from paralysis the mean length was less, due to a preponderance of small, new-formed clusters. These observations show that development of new endplates, which is thought to reflect the development of new muscle cells, is halted in paralysed muscles, and recovery from paralysis is associated with the generation of many new endplates. (iv) J-clusters appeared, but failed to grow, in aneural muscles. In muscles denervated during the later stages of gestation, analysis of the distribution of J-cluster lengths shows that new clusters failed to appear, and existing clusters showed little or no increase in length after the time of removal of the nerve. (v) EJ-clusters form by aggregation of dispersed receptors, and their mean length increases with time. They do not appear to be stable entities, and are removed within 2 d of recovery from paralysis. In paralysed muscles, with both J-clusters and EJclusters present, only J-clusters attract nerve sprouts or become innervated. (vi) A curve is derived showing development of the total number of synaptic terminals in a muscle. This number increases during days 13-18 of gestation, reaching a peak of about 170 % of the adult value during dl8 and d l9 of gestation. There are two episodes of terminal elimination, one during days 19-21 of gestation, and another about 2 weeks postnatally. During the first postnatal week the number of terminals remains constant at about 140% of the adult number, while the average number of inputs per fibre goes down and the number of muscle fibres increases. (vii) Innervation is essential for muscle development. Motoneurons cannot regulate the number of muscle fibres by requiring a simple one-to-one relation between nerve terminal and muscle fibre, and if their role is regulatory as well as supportive of muscle development then some more complex relationship between nerve terminals and developing myotubes must be postulated.

scholarly journals Myogenic conversion of mammalian fibroblasts induced by differentiating muscle cells

1995 ◽  
Vol 108 (8) ◽  
pp. 2733-2739 ◽  
Author(s):  
G. Salvatori ◽  
L. Lattanzi ◽  
M. Coletta ◽  
S. Aguanno ◽  
E. Vivarelli ◽  
...  
Keyword(s):  
Muscle Fibre ◽  
Striated Muscle ◽  
Muscle Cells ◽  
Cell Types ◽  
Sole Source ◽  
Cell Interaction ◽  
C2c12 Cells ◽  
Membrane Function ◽  
Beta Galactosidase

Somite-derived skeletal myoblasts are supposed to be the sole source of muscle fibre nuclei during pre- and postnatal development, but evidence is accumulating for unorthodox contributions to muscle fibre nuclei from other cell types. For example, in tissue culture, fibroblasts can fuse with dysgenic myoblasts and restore correct membrane function. We report here the results of a series of experiments investigating this phenomenon and its possible mechanism. 10T1/2 cells, infected with a replication defective retrovirus encoding the bacterial enzyme beta-galactosidase, fused to form beta-galactosidase positive, differentiated myotubes when cocultured with differentiating uninfected C2C12 or primary myogenic cells, but this did not occur when they were cocultured with other cells such as 3T3 fibroblasts or PC12 pheochromocytoma cells. Myogenic conversion ranged from 1 to 10% of the 10T1/2 cell population and required close cell interaction between the different cells types: it was not induced by conditioned medium or extracellular matrix deposited by C2C12 cells. Myogenic conversion was also observed in vivo, after injection of similarly infected 10T1/2 cells into regenerating muscle. Conversion was seen also after coculture of uninfected 10T1/2 cells with primary chick myoblasts, thus demonstrating that it was not dependent upon viral infection and that there is no species or class barrier in this phenomenon. Primary fibroblasts, isolated from different organs of transgenic mice carrying a Lac Z marker under the control of a muscle-specific promoter, restricting beta-galactosidase expression to striated muscle cells, also underwent myogenic conversion, when cocultured with C2C12 myoblasts.(ABSTRACT TRUNCATED AT 250 WORDS)

Visualization of satellite cells in living muscle fibres of the frog

1980 ◽  
Vol 209 (1177) ◽  
pp. 563-568 ◽  
Keyword(s):  
Electron Microscopy ◽  
Horseradish Peroxidase ◽  
Muscle Fibre ◽  
Satellite Cells ◽  
Light Microscope ◽  
Muscle Cells ◽  
Fibre Axis ◽  
Muscle Fibres ◽  
Single Fibres

Satellite cells were visualized in living muscle fibres of the frog. Single fibres or bundles consisting of a few fibres were isolated after treatment with collagenase, and viewed under the light microscope. Subsequent electron microscopy of identified cells confirmed that they were satellite muscle cells. Under the light microscope, satellite cells appear as fusiform cells, tapering into long fine processes usually orientated parallel to the muscle fibre axis. Horseradish peroxidase injected into the muscle fibre was not transferred to the satellite cells.

Relaxation Rate of Constituent Muscle-Fibre Types in Human Quadriceps

1979 ◽  
Vol 56 (1) ◽  
pp. 47-52 ◽  
Author(s):  
C. M. Wiles ◽  
A. Young ◽  
D. A. Jones ◽  
R. H. T. Edwards
Keyword(s):  
Relaxation Rate ◽  
Muscle Fibre ◽  
Human Subjects ◽  
Muscle Fibre Types ◽  
Muscle Fibres ◽  
Isometric Contractions ◽  
Type I ◽  
Type Ii ◽  
Fibre Type Composition

1. Muscle fibres may be subdivided into type I (with slow-twitch contractile properties) and type II (fast-twitch) depending on their myosin adenosine triphosphatase activity. In voluntary isometric contractions type I fibres are utilized at low forces (<20% of maximum) whereas type II fibres are recruited in addition at high forces. This physiological recruitment order has enabled us to measure the relaxation rate of type I and II fibres in vivo in normal human subjects. 2. Relaxation rate was measured in 16 subjects from low (10% of maximum) and maximum isometric quadriceps contractions and the muscle-fibre type composition determined from needle-biopsy specimens in 10 subjects. The relaxation rate of type II fibres was calculated to be twice as fast as that of type I. 3. It was not possible to estimate, from studies in 33 quadriceps muscles (25 normal subjects), the contribution of type II fibres to overall fibre area from the relaxation rate as determined from electrically stimulated isometric contractions.

scholarly journals In vivo genome editing in mouse restores dystrophin expression in Duchenne muscular dystrophy patient muscle fibers

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Menglong Chen ◽  
Hui Shi ◽  
Shixue Gou ◽  
Xiaomin Wang ◽  
Lei Li ◽  
...  
Keyword(s):  
Duchenne Muscular Dystrophy ◽  
Muscular Dystrophy ◽  
Mouse Model ◽  
Genome Editing ◽  
Large Scale ◽  
Gene Editing ◽  
High Efficiency ◽  
Muscle Fibers ◽  
Muscle Cells

Abstract Background Mutations in the DMD gene encoding dystrophin—a critical structural element in muscle cells—cause Duchenne muscular dystrophy (DMD), which is the most common fatal genetic disease. Clustered regularly interspaced short palindromic repeat (CRISPR)-mediated gene editing is a promising strategy for permanently curing DMD. Methods In this study, we developed a novel strategy for reframing DMD mutations via CRISPR-mediated large-scale excision of exons 46–54. We compared this approach with other DMD rescue strategies by using DMD patient-derived primary muscle-derived stem cells (DMD-MDSCs). Furthermore, a patient-derived xenograft (PDX) DMD mouse model was established by transplanting DMD-MDSCs into immunodeficient mice. CRISPR gene editing components were intramuscularly delivered into the mouse model by adeno-associated virus vectors. Results Results demonstrated that the large-scale excision of mutant DMD exons showed high efficiency in restoring dystrophin protein expression. We also confirmed that CRISPR from Prevotella and Francisella 1(Cas12a)-mediated genome editing could correct DMD mutation with the same efficiency as CRISPR-associated protein 9 (Cas9). In addition, more than 10% human DMD muscle fibers expressed dystrophin in the PDX DMD mouse model after treated by the large-scale excision strategies. The restored dystrophin in vivo was functional as demonstrated by the expression of the dystrophin glycoprotein complex member β-dystroglycan. Conclusions We demonstrated that the clinically relevant CRISPR/Cas9 could restore dystrophin in human muscle cells in vivo in the PDX DMD mouse model. This study demonstrated an approach for the application of gene therapy to other genetic diseases.

scholarly journals Stromal cells from human long-term marrow cultures are mesenchymal cells that differentiate following a vascular smooth muscle differentiation pathway

Blood ◽  
1993 ◽  
Vol 82 (1) ◽  
pp. 66-76 ◽  
Author(s):  
MC Galmiche ◽  
VE Koteliansky ◽  
J Briere ◽  
P Herve ◽  
P Charbord
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Stromal Cells ◽  
Muscle Cells ◽  
Mesenchymal Cells ◽  
Myoid Cells ◽  
Marrow Cultures

In human long-term marrow cultures connective tissue-forming stromal cells are an essential cellular component of the adherent layer where granulomonocytic progenitors are generated from week 2 onward. We have previously found that most stromal cells in confluent cultures were stained by monoclonal antibodies directed against smooth muscle- specific actin isoforms. The present study was carried out to evaluate the time course of alpha-SM-positive stromal cells and to search for other cytoskeletal proteins specific for smooth muscle cells. It was found that the expression of alpha-SM in stromal cells was time dependent. Most of the adherent spindle-shaped, vimentin-positive stromal cells observed during the first 2 weeks of culture were alpha- SM negative. On the contrary, from week 3 to week 7, most interdigitated stromal cells contained stress fibers whose backbone was made of alpha-SM-positive microfilaments. In addition, in confluent cultures, other proteins specific for smooth muscle were detected: metavinculin, h-caldesmon, smooth muscle myosin heavy chains, and calponin. This study confirms the similarity between stromal cells and smooth muscle cells. Moreover, our results reveal that cells in vivo with the phenotype closest to that of stromal cells are immature fetal smooth muscle cells and subendothelial intimal smooth muscle cells; a cell subset with limited development following birth but extensively recruited in atherosclerotic lesions. Stromal cells very probably derive from mesenchymal cells that differentiate along this distinctive vascular smooth muscle cell pathway. In humans, this differentiation seems crucial for the maintenance of granulomonopoiesis. These in vitro studies were completed by examination of trephine bone marrow biopsies from adults without hematologic abnormalities. These studies revealed the presence of alpha-SM-positive cells at diverse locations: vascular smooth muscle cells in the media of arteries and arterioles, pericytes lining capillaries, myoid cells lining sinuses at the abluminal side of endothelial cells or found within the hematopoietic logettes, and endosteal cells lining bone trabeculae. More or less mature cells of the granulocytic series were in intimate contact with the thin cytoplasmic extensions of myoid cells. Myoid cells may be the in vivo counterpart of stromal cells with the above-described vascular smooth muscle phenotype.

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