The role of autonomic pathways in peripheral apelin‐induced gastrointestinal dysmotility: involvement of the circumventricular organs

2020 ◽  
Author(s):  
Osman Sinen ◽  
Mehmet Bülbül
Keyword(s):  
Circumventricular Organs ◽  
Gastrointestinal Dysmotility ◽  
Autonomic Pathways

The Emerging Role of Helicobacter Pylori-Induced Metabolic Gastrointestinal Dysmotility and Neurodegeneration

2018 ◽  
Vol 17 (6) ◽  
Author(s):  
J. Kountouras ◽  
M. Boziki ◽  
S.A. Polyzos ◽  
P. Katsinelos ◽  
E. Gavalas ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastrointestinal Dysmotility

133 Role of Muscarinic-3 Receptor (M3-R) in Pathogenesis of Gastrointestinal Dysmotility in Systemic Sclerosis: Correlation With Disease Duration and Effects of IVIG

2016 ◽  
Vol 150 (4) ◽  
pp. S32
Author(s):  
Sumit Kumar ◽  
Jagmohan Singh ◽  
Fabian Mendoza ◽  
Sergio Jimenez ◽  
Anthony DiMarino ◽  
...  
Keyword(s):  
Systemic Sclerosis ◽  
Disease Duration ◽  
Gastrointestinal Dysmotility

Signaling the brain in systemic inflammation: role of sensory circumventricular organs

10.2741/1241 ◽  
2004 ◽  
Vol 9 (1-3) ◽  
pp. 290 ◽  
Author(s):  
Joachim Roth
Keyword(s):  
Systemic Inflammation ◽  
Circumventricular Organs ◽  
The Brain

Role of inducible nitric oxide synthase in gastrointestinal dysmotility in septic mice

2001 ◽  
Vol 120 (5) ◽  
pp. A290
Author(s):  
Benedicte Y. De Winter ◽  
Albert J. Bredenoord ◽  
Joris G. De Man ◽  
Tom G. Moreels ◽  
Arnold G. Herman ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Gastrointestinal Dysmotility ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Selected Contribution: Role of IL-6 in LPS-induced nuclear STAT3 translocation in sensory circumventricular organs during fever in rats

2002 ◽  
Vol 92 (6) ◽  
pp. 2657-2666 ◽  
Author(s):  
Eva-Maria Harré ◽  
Joachim Roth ◽  
Ulrich Pehl ◽  
Matthias Kueth ◽  
Rüdiger Gerstberger ◽  
...  
Keyword(s):  
Nuclear Translocation ◽  
Systemic Circulation ◽  
Circumventricular Organs ◽  
Strong Increase ◽  
Molecular Evidence ◽  
Febrile Response ◽  
Sensory Structures ◽  
Transcription 3 ◽  
Lps Treatment

Interleukin-6 (IL-6) is regarded as an endogenous mediator of lipopolysaccharide (LPS)-induced fever. IL-6 is thought to act on the brain at sites that lack a blood-brain barrier, the circumventricular organs (CVOs). Cells that are activated by IL-6 respond with nuclear translocation of the signal transducer and activator of transcription 3 molecule (STAT3) and can be detected by immunohistochemistry. We investigated whether the LPS-induced release of IL-6 into the systemic circulation was accompanied by a nuclear STAT3 translocation within the sensory CVOs. Treatment with LPS (100 μg/kg) led to a slight (1 h) and then a strong increase (2–8 h) in plasma IL-6 levels, which started to decline at the end of the febrile response. Administration of both pyrogens LPS and IL-6 (45 μg/kg) induced a febrile response with IL-6, causing a rather moderate fever compared with the LPS-induced fever. Nuclear STAT3 translocation in response to LPS was observed within the vascular organ of the lamina terminalis (OVLT) and the subfornical organ (SFO) 2 h after LPS treatment. To investigate whether this effect was mediated by IL-6, the cytokine itself was systemically applied and indeed an identical pattern of nuclear STAT3 translocation was observed. However, nuclear STAT3 translocation already occurred 1 h after IL-6 application and proved to be less effective compared with LPS treatment when analyzing OVLT and SFO cell numbers that showed nuclear STAT3 immunoreactivity after the respective pyrogen treatment. Our observations represent the first molecular evidence for an IL-6-induced STAT3-mediated genomic activation of OVLT and SFO cells and support the proposed role of these brain areas as sensory structures for humoral signals created by the activated immune system and resulting in the generation of fever.

Role of inducible nitric oxide synthase in gastrointestinal dysmotility in septic mice

2001 ◽  
Vol 120 (5) ◽  
pp. A290-A290
Author(s):  
B WINTER ◽  
A BREDENOORD ◽  
J MAN ◽  
T MOREELS ◽  
A HERMAN ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Gastrointestinal Dysmotility ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Role of Autonomic Pathways in Disuse Atrophy of Rat Parotid

1973 ◽  
Vol 143 (1) ◽  
pp. 19-22 ◽  
Author(s):  
H. D. Hall ◽  
C. A. Schneyer
Keyword(s):  
Disuse Atrophy ◽  
Autonomic Pathways ◽  
Rat Parotid

scholarly journals TREM Receptors Connecting Bowel Inflammation to Neurodegenerative Disorders

Cells ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 1124 ◽  
Author(s):  
Gianfranco Natale ◽  
Francesca Biagioni ◽  
Carla Letizia Busceti ◽  
Stefano Gambardella ◽  
Fiona Limanaqi ◽  
...  
Keyword(s):  
Neurodegenerative Disorders ◽  
Potential Role ◽  
Intestinal Bacteria ◽  
Circumventricular Organs ◽  
Leaky Gut ◽  
Inflammatory Processes ◽  
Inflammatory Bowel ◽  
Disease Specificity ◽  
The Brain

Alterations in Triggering Receptors Expressed on Myeloid cells (TREM-1/2) are bound to a variety of infectious, sterile inflammatory, and degenerative conditions, ranging from inflammatory bowel disease (IBD) to neurodegenerative disorders. TREMs are emerging as key players in pivotal mechanisms often concurring in IBD and neurodegeneration, namely microbiota dysbiosis, leaky gut, and inflammation. In conditions of dysbiosis, compounds released by intestinal bacteria activate TREMs on macrophages, leading to an exuberant pro-inflammatory reaction up to damage in the gut barrier. In turn, TREM-positive activated macrophages along with inflammatory mediators may reach the brain through the blood, glymphatic system, circumventricular organs, or the vagus nerve via the microbiota-gut-brain axis. This leads to a systemic inflammatory response which, in turn, impairs the blood-brain barrier, while promoting further TREM-dependent neuroinflammation and, ultimately, neural injury. Nonetheless, controversial results still exist on the role of TREM-2 compared with TREM-1, depending on disease specificity, stage, and degree of inflammation. Therefore, the present review aimed to provide an update on the role of TREMs in the pathophysiology of IBD and neurodegeneration. The evidence here discussed the highlights of the potential role of TREMs, especially TREM-1, in bridging inflammatory processes in intestinal and neurodegenerative disorders.

ON THE ROLE OF ARGININE VASOPRESSIN IN CIRCUMVENTRICULAR ORGANS

1982 ◽  
Vol 394 (1 The Brattlebo) ◽  
pp. 753-758 ◽  
Author(s):  
A. Negro-Vilar ◽  
W. K. Samson
Keyword(s):  
Arginine Vasopressin ◽  
Circumventricular Organs
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