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.

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.

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.

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.

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.

scholarly journals Disorders of Sleep and Aggression Trait in Women Associated: What Underlies Staying “Woke”?

2019 ◽  
Vol 1 (1) ◽  
Author(s):  
Hobgood DK
Keyword(s):  
Nervous System ◽  
Sleep Apnea ◽  
Sympathetic Nervous System ◽  
Dopamine System ◽  
Patient Falls ◽  
Online Test ◽  
Sympathetic Nervous ◽  
Sleep Centers ◽  
The Brain

Narcolepsy is a sleep disorder where the patient falls asleep unwillingly. It is thought to be related to hyper functioning central sleep centers in the brain. Sleep apnea is a disorder of breathing disruption during sleep. Genes of the dopamine system have been implicated with high dopamine: norepinephrine ratio. Since dopamine has also been associated with personality traits, the hypothesis we studied herein was that patients with narcolepsy and sleep apnea would score low in catecholamine settings causing aggression trait. We found that narcolepsy and sleep apnea diagnoses showed significantly lower aggression trait using an online test. The conclusion is that narcolepsy and sleep apnea patients are not aggressive in personality, and since aggressiveness is related to sympathetic nervous system activity, this would be predictable given the role of sympathetic nervous system in wakefulness.

scholarly journals The Brain-Heart Connection in Takotsubo Syndrome: The Central Nervous System, Sympathetic Nervous System, and Catecholamine Overload

2020 ◽  
Vol 2020 ◽  
pp. 1-5 ◽  
Author(s):  
Xiaopu Wang ◽  
Junyu Pei ◽  
Xinqun Hu
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Physiological Stress ◽  
Acute Chest Pain ◽  
Takotsubo Syndrome ◽  
The Central Nervous System ◽  
Sympathetic Nervous ◽  
As Stress ◽  
Artery Obstruction ◽  
The Brain

Takotsubo syndrome (TTS), also known as stress cardiomyopathy, is a type of acute heart failure syndrome triggered by intense psychological or physiological stress. TTS typically manifests as acute chest pain, dyspnea or syncope that mimics an acute myocardial infarction but does not involve coronary artery obstruction. The current understanding of the pathogenesis of TTS suggests that sympathetic nervous system (SNS) activation plays a central role. Specifically, stress can activate the SNS and lead to the over-release of catecholamine, which have toxic effects on myocardial tissue when present at excessive levels. However, the brain changes associated with TTS and the connection between the brain and the heart in patients with this disease remain unclear. In recent years, several published reports have revealed the role of this brain-heart connection in the pathogenesis of TTS. This review summarizes recent studies regarding SNS activation, catecholamine overload, and the brain-heart connection in patients with TTS from both pathophysiological and mechanistic aspects.

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