Regarding the relation of the sympathetic nervous system to the transverse striated muscles

1923 ◽  
Vol 19 (5) ◽  
pp. 3-8
Author(s):  
N. V. Puchkov
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Striated Muscle ◽  
Muscle Fibers ◽  
Nerve Fibers ◽  
Striated Muscles ◽  
Striated Muscle Fibers ◽  
Sympathetic Nervous ◽  
The Brain

In several articles published from 1909 to 1913, the Dutch scientist Boeke described in the transverse striated muscles nerve fibers accompanying the motor fleshy ones and ending in the motor plaques of the transverse striated muscle fibers. Examining the m. obliquus sup. of a cat in which the n. trochlearis was cut immediately at the exit from the brain, Voeke found the endings of sensory and motor fibers and preserved muscleless fibers (the cat died on the 4th day after the operation) reincarnated. On this basis, the author attributed the sympathetic origin to these fibers.

scholarly journals Central Fibroblast Growth Factor 21 Browns White Fat via Sympathetic Action in Male Mice

Endocrinology ◽  
2015 ◽  
Vol 156 (7) ◽  
pp. 2470-2481 ◽  
Author(s):  
Nicholas Douris ◽  
Darko M. Stevanovic ◽  
ffolliott M. Fisher ◽  
Theodore I. Cisu ◽  
Melissa J. Chee ◽  
...  
Keyword(s):  
Nervous System ◽  
Adipose Tissue ◽  
Growth Factor ◽  
Sympathetic Nervous System ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 21 ◽  
Fibroblast Growth ◽  
Male Mice ◽  
Sympathetic Nervous ◽  
The Brain

Fibroblast growth factor 21 (FGF21) has multiple metabolic actions, including the induction of browning in white adipose tissue. Although FGF21 stimulated browning results from a direct interaction between FGF21 and the adipocyte, browning is typically associated with activation of the sympathetic nervous system through cold exposure. We tested the hypothesis that FGF21 can act via the brain, to increase sympathetic activity and induce browning, independent of cell-autonomous actions. We administered FGF21 into the central nervous system via lateral ventricle infusion into male mice and found that the central treatment increased norepinephrine turnover in target tissues that include the inguinal white adipose tissue and brown adipose tissue. Central FGF21 stimulated browning as assessed by histology, expression of uncoupling protein 1, and the induction of gene expression associated with browning. These effects were markedly attenuated when mice were treated with a β-blocker. Additionally, neither centrally nor peripherally administered FGF21 initiated browning in mice lacking β-adrenoceptors, demonstrating that an intact adrenergic system is necessary for FGF21 action. These data indicate that FGF21 can signal in the brain to activate the sympathetic nervous system and induce adipose tissue thermogenesis.

Imbalance of central nitric oxide and reactive oxygen species in the regulation of sympathetic activity and neural mechanisms of hypertension

2011 ◽  
Vol 300 (4) ◽  
pp. R818-R826 ◽  
Author(s):  
Yoshitaka Hirooka ◽  
Takuya Kishi ◽  
Koji Sakai ◽  
Akira Takeshita ◽  
Kenji Sunagawa
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Brain Stem ◽  
Intracellular Signaling ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Sympathetic Nervous ◽  
The Brain

Nitric oxide (NO) and reactive oxygen species (ROS) play important roles in blood pressure regulation via the modulation of the autonomic nervous system, particularly in the central nervous system (CNS). In general, accumulating evidence suggests that NO inhibits, but ROS activates, the sympathetic nervous system. NO and ROS, however, interact with each other. Our consecutive studies and those of others strongly indicate that an imbalance between NO bioavailability and ROS generation in the CNS, including the brain stem, activates the sympathetic nervous system, and this mechanism is involved in the pathogenesis of neurogenic aspects of hypertension. In this review, we focus on the role of NO and ROS in the regulation of the sympathetic nervous system within the brain stem and subsequent cardiovascular control. Multiple mechanisms are proposed, including modulation of neurotransmitter release, inhibition of receptors, and alterations of intracellular signaling pathways. Together, the evidence indicates that an imbalance of NO and ROS in the CNS plays a pivotal role in the pathogenesis of hypertension.

scholarly journals Sympathetic Nervous System Control of Carbon Tetrachloride-Induced Oxidative Stress in Liver throughα-Adrenergic Signaling

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Jung-Chun Lin ◽  
Yi-Jen Peng ◽  
Shih-Yu Wang ◽  
Mei-Ju Lai ◽  
Ton-Ho Young ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Nervous System ◽  
Carbon Tetrachloride ◽  
Sympathetic Nervous System ◽  
Nerve Fibers ◽  
Adrenergic Signaling ◽  
Adrenergic Antagonist ◽  
Sympathetic Nervous

In addition to being the primary organ involved in redox cycling, the liver is one of the most highly innervated tissues in mammals. The interaction between hepatocytes and sympathetic, parasympathetic, and peptidergic nerve fibers through a variety of neurotransmitters and signaling pathways is recognized as being important in the regulation of hepatocyte function, liver regeneration, and hepatic fibrosis. However, less is known regarding the role of the sympathetic nervous system (SNS) in modulating the hepatic response to oxidative stress. Our aim was to investigate the role of the SNS in healthy and oxidatively stressed liver parenchyma. Mice treated with 6-hydroxydopamine hydrobromide were used to realize chemical sympathectomy. Carbon tetrachloride (CCl4) injection was used to induce oxidative liver injury. Sympathectomized animals were protected from CCl4induced hepatic lipid peroxidation-mediated cytotoxicity and genotoxicity as assessed by 4-hydroxy-2-nonenal levels, morphological features of cell damage, and DNA oxidative damage. Furthermore, sympathectomy modulated hepatic inflammatory response induced by CCl4-mediated lipid peroxidation. CCl4induced lipid peroxidation and hepatotoxicity were suppressed by administration of anα-adrenergic antagonist. We conclude that the SNS provides a permissive microenvironment for hepatic oxidative stress indicating the possibility that targeting the hepaticα-adrenergic signaling could be a viable strategy for improving outcomes in patients with acute hepatic injury.

Medulloblastoma with striated muscle fibers

1973 ◽  
Vol 38 (5) ◽  
pp. 642-646 ◽  
Author(s):  
Anthony J. Lewis
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Striated Muscle ◽  
Muscle Fibers ◽  
Malignant Gliomas ◽  
The Body ◽  
Content Type ◽  
Striated Muscle Fibers ◽  
Fine Print ◽  
Stimulation Of

✓ A case is reported in which a medulloblastoma showed evidence of striated muscle fibers. Fifteen additional cases of primary central nervous system (CNS) tumor containing muscle fibers (excluding teratomas) are reviewed. These tumors appear to be of mesenchymal, rather than teratoid, origin, and to be related to embryonal sarcomas (mesenchymomas) in other parts of the body. It is postulated that the presence of such fibers in malignant gliomas may be due to rhabdomyoblast-inducing action of mesenchyme, analogous to the fibroblastic stimulation observed in desmoplastic medulloblastomas, and the massive stimulation of perivascular tissue often associated with undifferentiated astrocytomas.

L-Dopa metabolism in genetically hypertensive mice: effect of pargyline

1987 ◽  
Vol 65 (12) ◽  
pp. 2390-2395 ◽  
Author(s):  
Nguyen T. Buu ◽  
Johanne Duhaime ◽  
Karoly Racz ◽  
Otto Kuchel ◽  
Gunther Schlager
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Monoamine Oxidase ◽  
Hydroxylase Activity ◽  
Sympathetic Nervous ◽  
The Relationship ◽  
The Brain ◽  
Genetically Hypertensive

This study on the role of the sympathetic nervous system in the development of hypertension involves the measurement of dopamine and norepinephrine accumulation in various tissues of the hypertensive and random-bred normotensive strains of mice at basal levels, and following a pargyline–L-dopa treatment. Under such a treatment, designed to suppress the homeostatic action of monoamine oxidase and to better expose the relationship between dopamine and norepinephrine, the brain and heart of the hypertensive mice accumulated more dopamine than the normotensive mice. There was a significantly lower norepinephrine accumulation in the heart of the hypertensive mice in spite of comparable dopamine-β-hydroxylase activity in this tissue between the two strains of mice. Under the pargyline–L-dopa treatment, the brain and heart of the older mice in both hypertensive and normotensive strains accumulated significantly (p < 0.05) more dopamine than those of their younger counterparts, while their norepinephrine accumulation remained unchanged. The results demonstrated different patterns of response of dopamine and norepinephrine in the development of hypertension.

scholarly journals Dr. Malaisé. Dorsal tabes and Graves' pseudo-fever. Tabes und Pseudo-Basedow. Monatschr. f. Psych. und Neurol. 1908-2

1909 ◽  
Vol XVI (1) ◽  
pp. 188-188
Author(s):  
A. Sholomovich
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Dry Mouth ◽  
Graves Disease ◽  
Sympathetic Nervous ◽  
The Brain

Based on the study of two cases of dry mouth cn. of the brain, with symptoms of Graves' disease, the author concludes: in isolated cases of tabes, a disease of the sympathetic nervous system is added, which gives clearly expressed symptoms, especially when the cervical n. sympathies.

Modulation of Dental Inflammation by the Sympathetic Nervous System

2006 ◽  
Vol 85 (6) ◽  
pp. 488-495 ◽  
Author(s):  
S.R. Haug ◽  
K.J. Heyeraas
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Inflammatory Cytokines ◽  
Dental Pulp ◽  
Inflammatory Cells ◽  
Sympathetic Nerves ◽  
Nerve Fibers ◽  
Dental Tissues ◽  
Reparative Dentin ◽  
Sympathetic Nervous

Recent findings have indicated that immune responses are subjected to modulation by the sympathetic nervous system (SNS). Moreover, the findings show that the SNS inhibits the production of pro-inflammatory cytokines, while stimulating the production of anti-inflammatory cytokines. The present review is an attempt to summarize the current results on how the SNS affects inflammation in dental tissues. In dental tissues, it has been found that the SNS is significant for recruitment of inflammatory cells such as CD 43+ granulocytes. Sympathetic nerves appear to have an inhibitory effect on osteoclasts, odontoclasts, and on IL-1α production. The SNS stimulates reparative dentin production, since reparative dentin formation was reduced after sympathectomy. Sprouting of sympathetic nerve fibers occurs in chronically inflamed dental pulp, and neural imbalance caused by unilateral sympathectomy recruits immunoglobulin-producing cells to the dental pulp. In conclusion, this article presents evidence in support of interactions between the sympathetic nervous system and dental inflammation.

Glucose increases rat plasma norepinephrine levels by direct action on the brain

1991 ◽  
Vol 261 (6) ◽  
pp. R1351-R1357 ◽  
Author(s):  
B. E. Levin
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Plasma Glucose ◽  
Direct Action ◽  
Rat Plasma ◽  
Plasma Norepinephrine ◽  
Intravenous Bolus ◽  
Intravenous Glucose ◽  
Sympathetic Nervous ◽  
The Brain

The hypothesis that glucose can selectively activate the sympathetic nervous system (SNS) by direct action on the brain was tested using plasma norepinephrine (NE) and epinephrine (Epi) responses to intracarotid and intravenous glucose injections as indexes of SNS and adrenal medullary responses, respectively. Intracarotid glucose bolus injections (0.1 g/kg) transiently raised plasma glucose (22%) and insulin (98%) levels at 2 min and increased plasma NE, but not Epi, levels from 2 to 60 min. Areas under the NE curve were 700% higher than equiosmolar doses of mannitol. An intravenous glucose bolus (1 g/kg) gave quantitatively similar but delayed (30 min) NE responses to the 0.1 g/kg intracarotid dose but raised plasma glucose 500% and insulin 1,700% above baseline at 2 min postinjection. Slow intracarotid glucose infusions for 60 min at 4 mg.kg-1.min-1 raised plasma NE levels from 30 to 60 min with 250% higher areas under the NE curve than the intracarotid and intravenous bolus doses but without a change in plasma glucose, insulin, or Epi levels. Infusions at 6 mg.kg-1.min-1 transiently raised plasma NE levels at 30 min without altering glucose, insulin, or Epi levels. These results suggest that glucose alone can produce a selective, delayed SNS activation by a direct action on the brain.

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