Beta-Endorphin Response to an Acute Pain Stimulus
Male; Pain Measurement; Time Factors; Reproducibility of Results; Animals; Mice; Acute Disease; Biomarkers of Pain; Physical Stimulation; Animal; beta-Endorphin/analysis/metabolism/secretion; Biological Markers/analysis/blood; Disease Models; Inbred DBA; Neurochemistry/methods; Pain/blood/physiopathology; Radioimmunoassay/methods; Up-Regulation/physiology
The timing of the measurement of biological samples (e.g. biomarkers) is not always standardized. Biomarkers are the focus of many recent studies and treatments. The purpose of this study was to determine the timing of the release of beta-endorphin (BE), a possible biomarker, after exposure to pain and/or handling stress in order to standardize measurements. Mouse plasma was collected for BE analysis following handling i.e. being picked up by the investigator, exposure to a painful (55 degrees C hot-plate), or exposure to a nonpainful stimulus (room temperature hot-plate). The groups exposed to either a painful or nonpainful stimulus released BE in response to the stimulus, but the duration of the response was longer in mice exposed to a painful stimulus than in mice exposed to a nonpainful stimulus. The BE in the mice exposed to a nonpainful stimulus peaked at 1 min and returned to baseline levels by 5 min while the BE response of the mice exposed to a painful stimulus peaked at 10 min and remained elevated for 25 min. The results of this study indicate that BE can be a biomarker for pain and handling stress, however, the timing of the measurement should differ.
Rasmussen NA; Farr LA
Journal Of Neuroscience Methods
2009
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Journal Article
<a href="http://doi.org/10.1016/j.jneumeth.2008.10.013" target="_blank" rel="noreferrer noopener">10.1016/j.jneumeth.2008.10.013</a>
Hypothalamo-pituitary-adrenal axis and chronic immune activation
Humans; Animals; Inflammation/immunology/physiopathology; Animal; Disease Models; Stress/immunology; Autoimmune Diseases/immunology/physiopathology; Corticosterone/secretion; Hypothalamo-Hypophyseal System/physiopathology; Immune System Diseases/physiopathology; Pituitary-Adrenal System/physiopathology
Corticosteroids have potent immunosuppressive and anti-inflammatory effects. Although corticosteroids are an important weapon in the clinical arsenal for treating inflammatory episodes, the mechanisms underlying the actions and regulation of endogenous corticosteroids remain obscure. In the late 1980s and early 1990s, a hypothesis was proposed that suggested that susceptibility to autoimmune disease was linked to a hypoactive hypothalamo-pituitary-adrenal (HPA) axis. It was further suggested that this defect in regulation of the HPA axis was situated at the level of the hypothalamus. This compelling hypothesis directly linked control of the HPA axis with susceptibility to disease rather than just severity of inflammation. The initial findings acted as a stimulus to further research, and over the next decade the hypothesis was tested. Recent studies suggest that the original hypothesis is in need of modification and that susceptibility is more complex and requires the involvement of more than a single parameter. These data are discussed together with recent developments concerning regulation of the HPA in disease in preclinical models and patients with rheumatoid arthritis. The latter studies in patients with rheumatoid arthritis provide evidence for the existence of a subpopulation of these patients with altered negative feedback regulation of the HPA axis.
2003
Harbuz MS; Chover-Gonzalez AJ; Jessop DS
Annals Of The New York Academy Of Sciences
2003
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Journal Article
<a href="http://doi.org/10.1111/j.1749-6632.2003.tb03141.x" target="_blank" rel="noreferrer">10.1111/j.1749-6632.2003.tb03141.x</a>
Inhibition of inflammatory pain by CRF at peripheral, spinal and supraspinal sites: involvement of areas coexpressing CRF receptors and opioid peptides
Male; Pain Measurement; Animals; Rats; Biomarkers of Pain; Dose-Response Relationship; Drug; Receptors; Freund's Adjuvant; Wistar; Animal; Disease Models; Analgesics/administration & dosage; Drug Administration Routes; Pain Threshold/drug effects; Brain/drug effects/metabolism; Spinal Cord/drug effects/metabolism; Corticotropin-Releasing Hormone/administration & dosage; Opioid Peptides/metabolism; Corticotropin-Releasing Hormone/metabolism; Ganglia; Hormone Antagonists/administration & dosage; Inflammation/chemically induced/complications; Pain/drug therapy/etiology/pathology; Sciatic Nerve/pathology; Spinal/drug effects/metabolism
There is conflicting evidence on the antinociceptive effects of corticotropin-releasing factor (CRF) along the neuraxis of pain transmission and the responsible anatomical sites of CRF's action at the level of the brain, spinal cord and periphery. In an animal model of tonic pain, that is, Freunds complete adjuvant (FCA) hindpaw inflammation, we systematically investigated CRF's ability to modulate inflammatory pain at those three levels of pain transmission by algesiometry following the intracerebroventricular, intrathecal, and intraplantar application of low, systemically inactive doses of CRF. At each level, CRF elicits potent antinociceptive effects, which are dose dependent and antagonized by local, but not systemic CRF receptor antagonist alpha-helical CRF indicating CRF receptor specificity. Consistently, we have identified by immunohistochemistry multiple brain areas, inhibitory interneurons within the dorsal horn of the spinal cord as well as immune cells within subcutaneous tissue--but not peripheral sensory neurons--that coexpress both CRF receptors and opioid peptides. In line with these anatomical findings, local administration of CRF together with the opioid receptor antagonist naloxone dose-dependently reversed CRF's antinociceptive effects at each of these three levels of pain transmission. Therefore, local application of low, systemically inactive doses of CRF at the level of the brain, spinal cord and periphery inhibits tonic inflammatory pain most likely through an activation of CRF receptors on cells that coexpress opioid peptides which results in opioid-mediated pain inhibition. Future studies have to delineate whether endogenous CRF at these three levels contributes to the body's response to cope with the stressful stimulus pain in an opioid-mediated manner.
2007
Mousa SA; Bopaiah CP; Richter JF; Yamdeu RS; Schafer M
Neuropsychopharmacology
2007
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Journal Article
<a href="http://doi.org/10.1038/sj.npp.1301393" target="_blank" rel="noreferrer">10.1038/sj.npp.1301393</a>