scholarly journals The Skin Microbiota and Itch: Is There a Link?

2020 ◽  
Vol 9 (4) ◽  
pp. 1190
Author(s):  
Hei Sung Kim ◽  
Gil Yosipovitch

Itch is an unpleasant sensation that emanates primarily from the skin. The chemical mediators that drive neuronal activity originate from a complex interaction between keratinocytes, inflammatory cells, nerve endings and the skin microbiota, relaying itch signals to the brain. Stress also exacerbates itch via the skin–brain axis. Recently, the microbiota has surfaced as a major player to regulate this axis, notably during stress settings aroused by actual or perceived homeostatic challenge. The routes of communication between the microbiota and brain are slowly being unraveled and involve neurochemicals (i.e., acetylcholine, histamine, catecholamines, corticotropin) that originate from the microbiota itself. By focusing on itch biology and by referring to the more established field of pain research, this review examines the possible means by which the skin microbiota contributes to itch.

2009 ◽  
Vol 18 (4) ◽  
pp. 237-241 ◽  
Author(s):  
Robert R. Edwards ◽  
Claudia Campbell ◽  
Robert N. Jamison ◽  
Katja Wiech

The biopsychosocial model treats pain as resulting from a complex interaction of biological, psychological, and social factors. Individual differences in approaches to coping with pain-related symptoms are important determinants of pain-related outcomes, and are often classified under the “psychological” category within the biopsychosocial model. However, engagement in various cognitive, affective, and behavioral pain-coping strategies appears to exert biological effects, which we review here. Pain-coping activities such as catastrophizing, distracting oneself from pain sensations, or reappraisal of pain may exert effects on activity in a variety of pain-processing and pain-modulatory circuits within the brain, as well affect the functioning of neuromuscular, immune, and neuroendocrine systems. The interface between pain-related neurobiology and the use of specific pain-coping techniques represents an important avenue for future pain research.


Author(s):  
Sara Keränen ◽  
Santeri Suutarinen ◽  
Rahul Mallick ◽  
Johanna P. Laakkonen ◽  
Diana Guo ◽  
...  

Abstract Background Brain arteriovenous malformations (bAVM) may rupture causing disability or death. BAVM vessels are characterized by abnormally high flow that in general triggers expansive vessel remodeling mediated by cyclo-oxygenase-2 (COX2), the target of non-steroidal anti-inflammatory drugs. We investigated whether COX2 is expressed in bAVMs and whether it associates with inflammation and haemorrhage in these lesions. Methods Tissue was obtained from surgery of 139 bAVMs and 21 normal Circle of Willis samples. The samples were studied with immunohistochemistry and real-time quantitative polymerase chain reaction (RT-PCR). Clinical data was collected from patient records. Results COX2 expression was found in 78% (109/139) of the bAVMs and localized to the vessels’ lumen or medial layer in 70% (95/135) of the bAVMs. Receptors for prostaglandin E2, a COX2-derived mediator of vascular remodeling, were found in the endothelial and smooth muscle cells and perivascular inflammatory cells of bAVMs. COX2 was expressed by infiltrating inflammatory cells and correlated with the extent of inflammation (r = .231, p = .007, Spearman rank correlation). COX2 expression did not associate with haemorrhage. Conclusion COX2 is induced in bAVMs, and possibly participates in the regulation of vessel wall remodelling and ongoing inflammation. Role of COX2 signalling in the pathobiology and clinical course of bAVMs merits further studies.


2021 ◽  
Vol 22 (7) ◽  
pp. 3330
Author(s):  
Mehdi Eshraghi ◽  
Aida Adlimoghaddam ◽  
Amir Mahmoodzadeh ◽  
Farzaneh Sharifzad ◽  
Hamed Yasavoli-Sharahi ◽  
...  

Alzheimer’s disease (AD) is a debilitating neurological disorder, and currently, there is no cure for it. Several pathologic alterations have been described in the brain of AD patients, but the ultimate causative mechanisms of AD are still elusive. The classic hallmarks of AD, including am-yloid plaques (Aβ) and tau tangles (tau), are the most studied features of AD. Unfortunately, all the efforts targeting these pathologies have failed to show the desired efficacy in AD patients so far. Neuroinflammation and impaired autophagy are two other main known pathologies in AD. It has been reported that these pathologies exist in AD brain long before the emergence of any clinical manifestation of AD. Microglia are the main inflammatory cells in the brain and are considered by many researchers as the next hope for finding a viable therapeutic target in AD. Interestingly, it appears that the autophagy and mitophagy are also changed in these cells in AD. Inside the cells, autophagy and inflammation interact in a bidirectional manner. In the current review, we briefly discussed an overview on autophagy and mitophagy in AD and then provided a comprehensive discussion on the role of these pathways in microglia and their involvement in AD pathogenesis.


2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Susumu Takahashi ◽  
Takumi Hombe ◽  
Riku Takahashi ◽  
Kaoru Ide ◽  
Shinichiro Okamoto ◽  
...  

Abstract Background Salmonids return to the river where they were born in a phenomenon known as mother-river migration. The underpinning of migration has been extensively examined, particularly regarding the behavioral correlations of external environmental cues such as the scent of the mother-river and geomagnetic compass. However, neuronal underpinning remains elusive, as there have been no biologging techniques suited to monitor neuronal activity in the brain of large free-swimming fish. In this study, we developed a wireless biologging system to record extracellular neuronal activity in the brains of free-swimming salmonids. Results Using this system, we recorded multiple neuronal activities from the telencephalon of trout swimming in a rectangular water tank. As proof of principle, we examined the activity statistics for extracellular spike waveforms and timing. We found cells firing maximally in response to a specific head direction, similar to the head direction cells found in the rodent brain. The results of our study suggest that the recorded signals originate from neurons. Conclusions We anticipate that our biologging system will facilitate a more detailed investigation into the neural underpinning of fish movement using internally generated information, including responses to external cues.


Renal Failure ◽  
1999 ◽  
Vol 21 (5) ◽  
pp. 551-554
Author(s):  
Hiroshi Tanaka ◽  
Hideki Hirakata ◽  
Hidetoshi Kanai ◽  
Itsuko Ishida ◽  
Masatoshi Fujishima

Author(s):  
Saleh A Othman ◽  

Background: Blood flow to the brain is in parallel with brain metabolism in almost all brain disorders except in brain tumors and therefore regional cerebral blood flow can be used as a marker of metabolic brain activity and hence it is closely linked to neuronal activity, the activity distribution is presumed to reflect neuronal activity levels in different areas of the brain. Purpose: The aim of this work is to demonstrate to pediatrician in general and pediatric neurologist in particular the variations in cerebral perfusion during normal development which should be taken into consideration at the time of interpreting SPECT brain perfusion scan in different pediatric brain disorders. Method: Brain SPECT was performed 10 minutes after an intravenous injection of 11.1 MBq/kg (0.3 mCi/kg), and the minimum dose is 185 MBq (5 mCi) of 99mTc-HMPAO (4). Results: This was a retrospective analysis of SPECT brain perfusion scan of pediatric patients performed between October 2015 and December 2019 at our institution. We selected normal and abnormal studies in pediatric population with age range (5 months - 14 years). Conclusion: Although anatomic cross sectional imaging give details of neurological structural changes, SPECT perfusion mirrors indirectly both metabolic and neuronal activity changes. Therefore, accurate interpretation of SPECT perfusion will consolidate its role as part of the diagnostic protocol and used when the findings of other imaging modalities do not explain the symptoms or fail partially or completely in determining the etiology of brain disorders in pediatric patients.


2017 ◽  
Vol 372 (1715) ◽  
pp. 20160504 ◽  
Author(s):  
Megumi Kaneko ◽  
Michael P. Stryker

Mechanisms thought of as homeostatic must exist to maintain neuronal activity in the brain within the dynamic range in which neurons can signal. Several distinct mechanisms have been demonstrated experimentally. Three mechanisms that act to restore levels of activity in the primary visual cortex of mice after occlusion and restoration of vision in one eye, which give rise to the phenomenon of ocular dominance plasticity, are discussed. The existence of different mechanisms raises the issue of how these mechanisms operate together to converge on the same set points of activity. This article is part of the themed issue ‘Integrating Hebbian and homeostatic plasticity’.


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