Extracellular signal‐regulated kinases 2 (Erk2) and Erk5 in the central nervous system differentially contribute to central sensitization in male mice

2021 ◽  
Vol 99 (6) ◽  
pp. 1666-1688
Author(s):  
Fumihiro Matsuura ◽  
Yasushi Satoh ◽  
Sayako Itakura ◽  
Toru Morohashi ◽  
Masanori Kawaguchi ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Central Sensitization ◽  
Male Mice ◽  
Extracellular Signal ◽  
The Central Nervous System

scholarly journals NGF, Brain and Behavioral Plasticity

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Alessandra Berry ◽  
Erika Bindocci ◽  
Enrico Alleva
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Behavioral Plasticity ◽  
The Body ◽  
Trophic Factor ◽  
Brain Growth ◽  
Male Mice ◽  
Psychosocial Stressor ◽  
The Central Nervous System

Nerve Growth Factor (NGF) was initially studied for its role as a key player in the regulation of peripheral innervations. However, the successive finding of its release in the bloodstream of male mice following aggressive encounters and its presence in the central nervous system led to the hypothesis that variations in brain NGF levels, caused by psychosocial stressor, and the related alterations in emotionality, could be functional to the development of proper strategies to cope with the stressor itself and thus to survive. Years later this vision is still relevant, and the body of evidence on the role of NGF has been strengthened and expanded from trophic factor playing a role in brain growth and differentiation to a much more complex messenger, involved in psychoneuroendocrine plasticity.

Increased Number of Mast Cells in the Central Nervous System of Adult Male Mice Following Chronic Subordination Stress

1998 ◽  
Vol 12 (2) ◽  
pp. 123-133 ◽  
Author(s):  
Francesca Cirulli ◽  
Luana Pistillo ◽  
Luigi de Acetis ◽  
Enrico Alleva ◽  
Luigi Aloe
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Mast Cells ◽  
Adult Male ◽  
Male Mice ◽  
The Central Nervous System

Progesterone as a regulator of phosphorylation in the central nervous system

2010 ◽  
Vol 4 (3) ◽  
Author(s):  
Miguel A.R. Amorim ◽  
Christian Guerra-Araiza ◽  
Luis M. Garcia-Segura
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Glycogen Synthase ◽  
Progesterone Receptors ◽  
Phosphatase And Tensin Homolog ◽  
Microtubule Stabilization ◽  
Tensin Homolog ◽  
Extracellular Signal ◽  
The Central Nervous System ◽  
Phosphoinositide 3 Kinase

AbstractProgesterone exerts a variety of actions in the central nervous system under physiological and pathological conditions. As in other tissues, progesterone acts in the brain through classical progesterone receptors and through alternative mechanisms. Here, we review the role of progesterone as a regulator of kinases and phosphatases, such as extracellular-signal regulated kinases, phosphoinositide 3-kinase, Akt, glycogen synthase kinase 3, protein phosphatase 2A and phosphatase and tensin homolog deleted on chromosome 10. In addition, we analyzed the effects of progesterone on the phosphorylation of Tau, a protein that is involved in microtubule stabilization in neurons.

scholarly journals Lack of Evidence for Central Sensitization in Idiopathic, Non-Traumatic Neck Pain: A Systematic Review

2015 ◽  
Vol 3;18 (3;5) ◽  
pp. 223-235
Author(s):  
Jo Nijs
Keyword(s):  
Systematic Review ◽  
Central Nervous System ◽  
Chronic Pain ◽  
Nervous System ◽  
Neck Pain ◽  
Central Sensitization ◽  
Case Control ◽  
Case Control Studies ◽  
The Central Nervous System ◽  
Pain Patients

Background: Chronic neck pain is a common problem with a poorly understood pathophysiology. Often no underlying structural pathology can be found and radiological imaging findings are more related to age than to a patient’s symptoms. Besides its common occurrence, chronic idiopathic neck pain is also very disabling with almost 50% of all neck pain patients showing moderate disability at long-term follow-up. Central sensitization (CS) is defined as “an amplification of neural signaling within the central nervous system that elicits pain hypersensitivity,” “increased responsiveness of nociceptive neurons in the central nervous system to their normal or subthreshold afferent input,” or “an augmentation of responsiveness of central neurons to input from unimodal and polymodal receptors.” There is increasing evidence for involvement of CS in many chronic pain conditions. Within the area of chronic idiopathic neck pain, there is consistent evidence for the presence and clinical importance of CS in patients with traumatic neck pain, or whiplash-associated disorders. However, the majority of chronic idiopathic neck pain patients are unrelated to a traumatic injury, and hence are termed chronic idiopathic non-traumatic neck pain. When comparing whiplash with idiopathic non-traumatic neck pain, indications for different underlying mechanisms are found. Objective: The goal of this article was to review the existing scientific literature on the role of CS in patients with chronic idiopathic non-traumatic neck pain. Study Design: Systematic review. Setting: All selected studies were case control studies. Methods: A systematic search of existing, relevant literature was performed via the electronic databases Medline, Embase, Web of Science, Cinahl, PubMed, and Google Scholar. All titles and abstracts were checked to identify relevant articles. An article was considered eligible if it met following inclusion criteria: (1) participants had to be human adults (> 18 years) diagnosed with idiopathic non-traumatic chronic (present for at least 3 months) neck pain; (2) papers had to report outcomes related to CS; and (3) articles had to be full-text reports or original research (no abstracts, case-reports, reviews, meta-analysis, letters, or editorials). Results: Six articles were found eligible after screening the title, abstract and – when necessary – the full text for in- and exclusion criteria. All selected studies were case-control studies. Overall, results regarding the presence of CS were divergent. While the majority of patients with chronic traumatic neck pain (i.e. whiplash) are characterized by CS, this is not the case for patients with chronic idiopathic neck pain. The available evidence suggests that CS is not a major feature of chronic idiopathic neck pain. Individual cases might have CS pain, but further work should reveal how they can be characterized. Limitations: Very few studies available. Conclusions: Literature about CS in patients with chronic idiopathic non-traumatic neck pain is rare and results from the available studies provide an inconclusive message. CS is not a characteristic feature of chronic idiopathic and non-traumatic neck pain, but can be present in some individuals of the population. In the future a subgroup with CS might be defined, but based on current knowledge it is not possible to characterize this subgroup. Such information is important in order to provide targeted treatment. Key words: Central sensitization, hypersensitivity, chronic pain, neck pain, idiopathic, nontraumatic, pressure pain thresholds, review

scholarly journals Neuroinflammation and Central Sensitization in Chronic and Widespread Pain

2018 ◽  
Vol 129 (2) ◽  
pp. 343-366 ◽  
Author(s):  
Ru-Rong Ji ◽  
Andrea Nackley ◽  
Yul Huh ◽  
Niccolò Terrando ◽  
William Maixner
Keyword(s):  
Central Nervous System ◽  
Chronic Pain ◽  
Nervous System ◽  
Central Sensitization ◽  
Chronic Widespread Pain ◽  
Widespread Pain ◽  
New Therapeutic Approaches ◽  
Cytokines And Chemokines ◽  
The Central Nervous System ◽  
Widespread Chronic Pain

Abstract Chronic pain is maintained in part by central sensitization, a phenomenon of synaptic plasticity, and increased neuronal responsiveness in central pain pathways after painful insults. Accumulating evidence suggests that central sensitization is also driven by neuroinflammation in the peripheral and central nervous system. A characteristic feature of neuroinflammation is the activation of glial cells, such as microglia and astrocytes, in the spinal cord and brain, leading to the release of proinflammatory cytokines and chemokines. Recent studies suggest that central cytokines and chemokines are powerful neuromodulators and play a sufficient role in inducing hyperalgesia and allodynia after central nervous system administration. Sustained increase of cytokines and chemokines in the central nervous system also promotes chronic widespread pain that affects multiple body sites. Thus, neuroinflammation drives widespread chronic pain via central sensitization. We also discuss sex-dependent glial/immune signaling in chronic pain and new therapeutic approaches that control neuroinflammation for the resolution of chronic pain.

scholarly journals Function of Cathepsin K in the Central Nervous System of Male Mice is Independent of Its Role in the Thyroid Gland

2019 ◽  
Vol 40 (5) ◽  
pp. 695-710 ◽  
Author(s):  
Stephanie Dauth ◽  
Helena Rakov ◽  
Ruxandra F. Sîrbulescu ◽  
Iulian Ilieş ◽  
Jonas Weber ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Thyroid Gland ◽  
Cathepsin K ◽  
Male Mice ◽  
The Central Nervous System
Sign in / Sign up

Export Citation Format

Share Document