scholarly journals The all-or-none role of innervation in expression of apamin receptor and of apamin-sensitive Ca2+-activated K+ channel in mammalian skeletal muscle.

1985 ◽  
Vol 82 (7) ◽  
pp. 2188-2191 ◽  
Author(s):  
H. Schmid-Antomarchi ◽  
J. F. Renaud ◽  
G. Romey ◽  
M. Hugues ◽  
A. Schmid ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
K Channel ◽  
Mammalian Skeletal Muscle

Role of muscle fasciculations in the generation of myopathies in mammalian skeletal muscle

1992 ◽  
Vol 29 (2) ◽  
pp. 179-187 ◽  
Author(s):  
Michael Adler ◽  
Donald Hinman ◽  
C.Sue Hudson
Keyword(s):  
Skeletal Muscle ◽  
Mammalian Skeletal Muscle

scholarly journals PO-064 A potential role of stretch-activated channels in anabolic mechanotransduction in the atrophied rat soleus muscle

2018 ◽  
Vol 1 (3) ◽  
Author(s):  
Timur Mirzoev ◽  
Sergey Tyganov ◽  
Boris Shenkman
Keyword(s):  
Skeletal Muscle ◽  
Soleus Muscle ◽  
Contractile Function ◽  
Mammalian Skeletal Muscle ◽  
Mechanical Unloading ◽  
Mtorc1 Signaling ◽  
Significant Difference ◽  
Rat Soleus Muscle ◽  
Isolated Rat

Objective Prolonged immobilization or unloading of skeletal muscle causes muscle disuse atrophy, which is characterized by a reduction in muscle cross-sectional area and compromised contractile function. To date, the mechanisms of anabolic mechanotransduction in the atrophied mammalian skeletal muscle remain poorly understood. The aim of the present study was to assess a possible role of stretch-activated ion channels (SAC) in the propagation of a mechanical signal to anabolic signaling and protein synthesis (PS) in an isolated rat soleus muscle following mechanical unloading. Methods The mechanical unloading was performed via hindlimb suspension (HS). Twenty-eight male Wistar rats weighing were randomly assigned to the following 4 groups (n=7/group): 1) vivarium control (C), 2) control + SAC inhibitor (gadolinium) (C+Gd3+), 3) 7-day HS (HS), 4) 7-day HS + SAC inhibitor (HS+Gd3+). Following unloading, an isolated rat soleus was placed in an organ culture medium and subjected to a bout of eccentric contractions (EC). Upon completion of the EC, muscles were collected for Western blot analyses to determine the content of the key anabolic markers. The rate of PS was measured by SUnSET technique. Results EC-induced increase in PS was significantly less in the HS and HS+ Gd3+ groups vs. the C group. There was no statistically significant difference between the HS and HS+ Gd3+ groups in terms of EC-induced increase in muscle PS. A decrease in EC-induced phosphorylation of p70S6K, 4E-BP1, RPS6 and GSK-3beta in the 7-day unloaded soleus treated with SAC inhibitor did not differ from that of the 7-day unloaded soleus without SAC blockade. Thus, the inhibition of SAC with gadolinium did not lead to further decline in EC-induced phosphorylation of the key anabolic markers and muscle PS. Conclusions The results of the study suggest that attenuation of mTORC1-signaling and PS in response to EC in unloaded soleus muscle may be associated with inactivation of SAC. The study was supported by the RFBR grant # 16-34-60055.

scholarly journals Role of extracellular [Ca2+] in fatigue of isolated mammalian skeletal muscle

1998 ◽  
Vol 84 (4) ◽  
pp. 1395-1406 ◽  
Author(s):  
Simeon P. Cairns ◽  
Wayne A. Hing ◽  
John R. Slack ◽  
Roland G. Mills ◽  
Denis S. Loiselle
Keyword(s):  
Skeletal Muscle ◽  
Action Potentials ◽  
Mammalian Skeletal Muscle ◽  
Control Solution ◽  
Tetanic Force ◽  
Complete Restoration ◽  
Slow Twitch ◽  
Fast Twitch ◽  
Strength Relationship

The possible role of altered extracellular Ca2+concentration ([Ca2+]o) in skeletal muscle fatigue was tested on isolated slow-twitch soleus and fast-twitch extensor digitorum longus muscles of the mouse. The following findings were made. 1) A change from the control solution (1.3 mM [Ca2+]o) to 10 mM [Ca2+]o, or to nominally Ca2+-free solutions, had little effect on tetanic force in nonfatigued muscle. 2) Almost complete restoration of tetanic force was induced by 10 mM [Ca2+]oin severely K+-depressed muscle (extracellular K+ concentration of 10–12 mM). This effect was attributed to a 5-mV reversal of the K+-induced depolarization and subsequent restoration of ability to generate action potentials (inferred by using the twitch force-stimulation strength relationship). 3) Tetanic force depressed by lowered extracellular Na+concentration (40 mM) was further reduced with 10 mM [Ca2+]o. 4) Tetanic force loss at elevated extracellular K+ concentration (8 mM) and lowered extracellular Na+concentration (100 mM) was partially reversed with 10 mM [Ca2+]oor markedly exacerbated with low [Ca2+]o. 5) Fatigue induced by using repeated tetani in soleus was attenuated at 10 mM [Ca2+]o(due to increased resting and evoked forces) and exacerbated at low [Ca2+]o. These combined results suggest, first, that raised [Ca2+]oprotects against fatigue rather than inducing it and, second, that a considerable depletion of [Ca2+]oin the transverse tubules may contribute to fatigue.

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