Faculty Opinions recommendation of The sympathetic nervous system regulates skeletal muscle motor innervation and acetylcholine receptor stability.

Author(s):  
William Phillips
2018 ◽  
Vol 225 (3) ◽  
Author(s):  
Anna C. Z. Rodrigues ◽  
Maria L. Messi ◽  
Zhong‐Min Wang ◽  
Martin C. Abba ◽  
Andrea Pereyra ◽  
...  

2021 ◽  
Vol 67 ◽  
pp. 101305
Author(s):  
Osvaldo Delbono ◽  
Anna Carolina Zaia Rodrigues ◽  
Henry Jacob Bonilla ◽  
Maria Laura Messi

1996 ◽  
Vol 270 (2) ◽  
pp. R462-R468 ◽  
Author(s):  
L. M. Larkin ◽  
J. B. Halter ◽  
M. A. Supiano

In this study, we tested the hypothesis that, in the male Fischer 344 x Brown Norway (F344xBN) rat, aging would be associated with an increase in sympathetic nervous system activity and a decrease in skeletal muscle beta-adrenergic-receptor (beta-AR) density and function. Radioligand-binding studies using [125I] iodocyanopindolol were done to evaluate beta-AR density (Bmax) and antagonist-binding affinity in gastrocnemius and cardiac muscle from 6-, 18-, and 28-mo-old male F344xBN rats. beta-AR function was measured as adenylyl cyclase (AC) activity stimulated by the beta-AR agonist isoproterenol (Iso, 10(-4) M). Basal arterial plasma norepinephrine (pNE) concentrations were higher in the 28-than in the 6- and 18-mo-old rats. Bmax was greatest and Iso-stimulated AC activity was unchanged in gastrocnemius muscle of the 28-mo-old age group. In contrast, there was an age-associated decrease in Bmax and Iso-stimulated AC activity in cardiac muscle. In conclusion, there was an age-associated increase in pNE concentrations in male F344xBN rats, suggesting an increase in sympathetic nervous system activity. In addition, there was an age-associated increase in skeletal muscle beta-AR density, whereas in skeletal muscle beta-AR-stimulated AC activity remained unchanged with age.


Endocrinology ◽  
2014 ◽  
Vol 155 (6) ◽  
pp. 2133-2143 ◽  
Author(s):  
Steven W. Yau ◽  
Belinda A. Henry ◽  
Vincenzo C. Russo ◽  
Glenn K. McConell ◽  
Iain J. Clarke ◽  
...  

Leptin is produced from white adipose tissue and acts primarily to regulate energy balance. Obesity is associated with leptin resistance and increased circulating levels of leptin. Leptin has recently been shown to influence levels of IGF binding protein-2 (IGFBP-2), a protein that is reduced in obesity and type 2 diabetes. Overexpression of IGFBP-2 protects against obesity and type 2 diabetes. As such, IGFBP-2 signaling may represent a novel pathway by which leptin regulates insulin sensitivity. We sought to investigate how leptin regulates skeletal muscle IGFBP-2 levels and to assess the impact of this on insulin signaling and glucose uptake. In vitro experiments were undertaken in cultured human skeletal myotubes, whereas in vivo experiments assessed the effect of intracerebroventricular leptin on peripheral skeletal muscle IGFBP-2 expression and insulin sensitivity in sheep. Leptin directly increased IGFBP-2 mRNA and protein in human skeletal muscle through both signal transducer and activator of transcription-3 and phosphatidylinositol 3-kinase signaling, in parallel with enhanced insulin signaling. Silencing IGFBP-2 lowered leptin- and insulin-stimulated protein kinase B phosphorylation and glucose uptake. In in vivo experiments, intracerebroventricular leptin significantly increased hind-limb skeletal muscle IGFBP-2, an effect completely blocked by concurrent peripheral infusion of a β-adrenergic blocking agent. Sheep receiving central leptin showed improvements in glucose tolerance and circulating insulin levels after an iv glucose load. In summary, leptin regulates skeletal muscle IGFBP-2 by both direct peripheral and central (via the sympathetic nervous system) mechanisms, and these likely impact on peripheral insulin sensitivity and glucose metabolism.


Endocrinology ◽  
2011 ◽  
Vol 152 (8) ◽  
pp. 3093-3102 ◽  
Author(s):  
W. Ramadan ◽  
A. Marsili ◽  
P. R. Larsen ◽  
A. M. Zavacki ◽  
J. E. Silva

Mice with ablation of the Thra gene have cold intolerance due to an as yet undefined defect in the activation of brown adipose tissue (BAT) uncoupling protein (UCP). They develop an alternate form of facultative thermogenesis, activated at temperatures below thermoneutrality and associated with hypermetabolism and reduced sensitivity to diet-induced obesity. A consistent finding in Thra-0/0 mice is increased type-2 iodothyronine deiodinase (D2) mRNA in skeletal muscle and other tissues. With an improved assay to measure D2 activity, we show here that this enzyme activity is increased in proportion to the mRNA and as a function of the ambient cold. The activation is mediated by the sympathetic nervous system in Thra-0/0, as it is in wild-type genotype mice, but the sympathetic nervous system effect is greater in Thra-0/0 mice. Using D2-ablated mice (Dio2−/−), we reported elsewhere and show here that, in spite of sharing a severe deficiency in BAT thermogenesis with Thra-0/0 and UCP1-knockout mice, they do not have an increase in oxygen consumption, and they gain more weight than wild-type controls when fed a high-fat diet. UCP3 mRNA is highly responsive to thyroid hormone, and it is increased in Thra-0/0 mice, particularly when fed high-fat diets. We show here that muscle UCP3 mRNA in hypothyroid Thra-0/0 mice is responsive to small dose-short regimens of T4, indicating a role for locally, D2-generated T3. Lastly, we show that bile acids stimulate not only BAT but also muscle D2 activity, and this is associated with stimulation of muscle UCP3 mRNA expression provided T4 is present. These observations strongly support the concept that enhanced D2 activity in Thra-0/0 plays a critical role in their alternate form of facultative thermogenesis, stimulating increased fat oxidation by increasing local T3 generation in skeletal muscle.


2009 ◽  
Vol 10 (6) ◽  
pp. 466-480 ◽  
Author(s):  
Tetsuya Shiuchi ◽  
Mohammad Shahidul Haque ◽  
Shiki Okamoto ◽  
Tsuyoshi Inoue ◽  
Haruaki Kageyama ◽  
...  

As a result of their experiments on normal, spinal and decerebrate animals Hunter and Royle (1924) concluded that the post-ganglionic fibres of the sympathetic nervous system constituted the efferent limb of the reflex arc subserving postural contraction in skeletal muscle. In a recent article (1931) the present author described a series of experiments on decerebrate cats in which Royle’s observation of diminished resistance to passive flexion in a sympathectomised “decerebrate” extensor muscle was confirmed, but the hypothesis that this was due to a “tonic” nervous influence of sympathetic axones on skeletal muscle fibres was denied. This denial was based on the fact that postural contraction was modified but not abolished by sympathectomy, and that the operation actually enhanced such proprioceptive reflexes as the shortening reaction and the crossed extensor reflex of Philippson (1905). Finally it was suggested that the diminished resistance of the extended “decerebrate” limb to passive flexion and the enhancement of those proprioceptive reflexes which, could be elicited by stretching the sympathectomised muscle were produced by a disturbance of the excitability of its proprioceptive end-organs. Denny-Brown (1928), after studying postural reflexes, has stated that the sympathetic nervous system is not essential to the stretch reflex, but he further stated that he was unable to discover any effect on general posture by excision of the sympathetic.


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