Effects of chronic stimulation on the size and speed of long-term denervated and innervated rat fast and slow skeletal muscles

1987 ◽  
Vol 130 (1) ◽  
pp. 115-131 ◽  
Author(s):  
R. HENNIG ◽  
T. LØMO
Keyword(s):  
Skeletal Muscles ◽  
Chronic Stimulation

scholarly journals Effects of long-term physical exercise on skeletal muscles in senescence-accelerated mice (SAMP8)

2018 ◽  
Vol 83 (3) ◽  
pp. 518-524 ◽  
Author(s):  
Kaho Takigawa ◽  
Rintaro Matsuda ◽  
Ran Uchitomi ◽  
Takumi Onishi ◽  
Yukino Hatazawa ◽  
...  
Keyword(s):  
Physical Exercise ◽  
Skeletal Muscles ◽  
Senescence Accelerated Mice

scholarly journals Transient enhancement of GLUT-4 levels in rat epitrochlearis muscle after exercise training

2000 ◽  
Vol 88 (6) ◽  
pp. 2240-2245 ◽  
Author(s):  
Thomas H. Reynolds ◽  
Joseph T. Brozinick ◽  
Lisa M. Larkin ◽  
Samuel W. Cushman
Keyword(s):  
Exercise Training ◽  
Protein Content ◽  
Glucose Transport ◽  
Skeletal Muscles ◽  
Transport Activity ◽  
Short Term ◽  
Glut 4 ◽  
Glucose Transport System ◽  
Female Wistar Rats

The purpose of the present study was to examine the effect of detraining on the glucose transport system after short-term swim training (5 days), long-term swim training (5 wk), and treadmill run training (5 wk). Skeletal muscles were isolated from female Wistar rats at 24 or 48 h posttraining. SST produces a 48% increase in GLUT-4 mRNA, a 30% increase in GLUT-4 protein, and a 60% increase in insulin-stimulated glucose transport activity at 24 h posttraining but not at 48 h posttraining. Similar to SST, long-term swim training produces a 60% increase in GLUT-4 mRNA and a 30% increase in GLUT-4 protein content at 24 h posttraining but not at 48 h posttraining. Finally, treadmill run training produces a transient 35% increase in GLUT-4 protein content that is completely reversed at 48 h after the last bout of exercise. These results demonstrate that the increase in GLUT-4 mRNA and GLUT-4 protein occurs during the first week of exercise training and is rapidly lost after training cessation. We believe that the transient enhancement in GLUT-4 protein after exercise training is due to a short GLUT-4 half-life, a process that is primarily regulated by pretranslational mechanisms.

scholarly journals Long-term regeneration of fast and slow murine skeletal muscles after induced injury by ACL myotoxin isolated fromAgkistrodon contortrix laticinctus (broad-banded copperhead) venom

1999 ◽  
Vol 254 (4) ◽  
pp. 521-533 ◽  
Author(s):  
Tania De F�tima Salvini ◽  
Cl�udio C�sar Morini ◽  
Heloisa Sobreiro Selistre De Ara�jo ◽  
Charlotte Ledbetter Ownby
Keyword(s):  
Skeletal Muscles

scholarly journals Agrin-like molecules at synaptic sites in normal, denervated, and damaged skeletal muscles.

1987 ◽  
Vol 105 (6) ◽  
pp. 2457-2469 ◽  
Author(s):  
N E Reist ◽  
C Magill ◽  
U J McMahan
Keyword(s):  
Monoclonal Antibodies ◽  
Neuromuscular Junction ◽  
Basal Lamina ◽  
Skeletal Muscles ◽  
Neuromuscular Junctions ◽  
Electric Organ ◽  
Synaptic Cleft ◽  
Cellular Components ◽  
Term Maintenance

Several lines of evidence have led to the hypothesis that agrin, a protein extracted from the electric organ of Torpedo, is similar to the molecules in the synaptic cleft basal lamina at the neuromuscular junction that direct the formation of acetylcholine receptor and acetylcholinesterase aggregates on regenerating myofibers. One such finding is that monoclonal antibodies against agrin stain molecules concentrated in the synaptic cleft of neuromuscular junctions in rays. In the studies described here we made additional monoclonal antibodies against agrin and used them to extend our knowledge of agrin-like molecules at the neuromuscular junction. We found that anti-agrin antibodies intensely stained the synaptic cleft of frog and chicken as well as that of rays, that denervation of frog muscle resulted in a reduction in staining at the neuromuscular junction, and that the synaptic basal lamina in frog could be stained weeks after degeneration of all cellular components of the neuromuscular junction. We also describe anti-agrin staining in nonjunctional regions of muscle. We conclude the following: (a) agrin-like molecules are likely to be common to all vertebrate neuromuscular junctions; (b) the long-term maintenance of such molecules at the junction is nerve dependent; (c) the molecules are, indeed, a component of the synaptic basal lamina; and (d) they, like the molecules that direct the formation of receptor and esterase aggregates on regenerating myofibers, remain associated with the synaptic basal lamina after muscle damage.

scholarly journals CREB regulates the expression of Type 1 Inositol 1,4,5-trisphosphate receptors

2021 ◽  
Author(s):  
Vikas Arige ◽  
Lara E. Terry ◽  
Sundeep Malik ◽  
Taylor R. Knebel ◽  
Larry E. Wagner ◽  
...  
Keyword(s):  
Long Term Effects ◽  
Ip3 Receptors ◽  
Chronic Stimulation ◽  
Interacting Protein ◽  
Post Translational Modifications ◽  
Over Expression ◽  
Pathological Conditions ◽  
Inositol 1,4,5 Trisphosphate

Inositol 1,4,5-trisphosphate (IP3) receptors (IP3Rs) play a central role in regulating intracellular calcium signals in response to a variety of internal/external cues. Dysregulation of IP3R signaling is the underlying cause for numerous pathological conditions. It is well established that the activities of IP3Rs are governed by several post-translational modifications including phosphorylation by protein kinase A (PKA). However, the long-term effects of PKA activation on expression of IP3R sub-types, remains largely unexplored. In this report, we investigate the effects of more chronic stimulation and tonic activity of PKA on the expression of IP3R sub-types. We demonstrate that the expression of IP3R1 is augmented upon prolonged activation of PKA or upon ectopic over-expression of CREB without altering IP3R2 and IP3R3 abundance. Conversely, inhibition of PKA or blocking CREB diminished IP3R1 expression. We also demonstrate that agonist-induced Ca2+-release mediated by IP3R1 is significantly attenuated upon blocking CREB. Moreover, CREB by regulating the expression of KRAS-induced actin-interacting protein (KRAP) ensures proper localization and licensing of IP3R1. Overall, we report a crucial role for CREB in governing both the expression and proper localization of IP3R1.

Reactive oxygen species participate in acute renal vasoconstrictor responses induced by ETA and ETB receptors

2008 ◽  
Vol 294 (4) ◽  
pp. F719-F728 ◽  
Author(s):  
Armin Just ◽  
Christina L. Whitten ◽  
William J. Arendshorst
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Long Term Effects ◽  
Vasomotor Tone ◽  
Chronic Stimulation ◽  
Renal Vasoconstriction ◽  
Oxidase Inhibition

Reactive oxygen species (ROS) play important roles in renal vasoconstrictor responses to acute and chronic stimulation by angiotensin II and norepinephrine, as well as in long-term effects of endothelin-1 (ET-1). Little is known about participation of ROS in acute vasoconstriction produced by ET-1. We tested the influence of NAD(P)H oxidase inhibition by apocynin [4 mg·kg−1·min−1, infused into the renal artery (ira)] on ETA and ETB receptor signaling in the renal microcirculation. Both receptors were stimulated by ET-1, ETA receptors by ET-1 during ETB antagonist BQ-788, and ETB by ETB agonist sarafotoxin 6C. ET-1 (1.5 pmol injected ira) reduced renal blood flow (RBF) 17 ± 4%. Apocynin raised baseline RBF (+10 ± 1%, P < 0.001) and attenuated the ET-1 response to 10 ± 2%, i.e., 35 ± 9% inhibition ( P < 0.05). Apocynin reduced ETA-induced vasoconstriction by 42 ± 12% ( P < 0.05) and that of ETB stimulation by 50 ± 8% ( P < 0.001). During nitric oxide (NO) synthase inhibition ( Nω-nitro-l-arginine methyl ester), apocynin blunted ETA-mediated vasoconstriction by 60 ± 8% ( P < 0.01), whereas its effect on the ETB response (by 87 ± 8%, P < 0.001) was even larger without than with NO present ( P < 0.05). The cell-permeable superoxide dismutase mimetic tempol (5 mg·kg−1·min−1 ira), which reduces O2− and may elevate H2O2, attenuated ET-1 responses similar to apocynin (by 38 ± 6%, P < 0.01). We conclude that ROS, O2− rather than H2O2, contribute substantially to acute renal vasoconstriction elicited by both ETA and ETB receptors and to basal renal vasomotor tone in vivo. This physiological constrictor action of ROS does not depend on scavenging of NO. In contrast, scavenging of O2− by NO seems to be more important during ETB stimulation.

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