WordNet

injurious to physical or mental health; "noxious chemical wastes"; "noxious ideas"

PrepTutorEJDIC

(健康上)有害な,身体に悪い / (道徳的に)有害な,不健全な
stimulusの複数形

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/04/26 17:16:13」(JST)

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A noxious stimulus is "an actually or potentially tissue damaging event."^[1] It is a prerequisite for nociception, which itself is a prerequisite for nociceptive pain.^[1]

Noxious stimuli can either be mechanical (e.g. pinching or other tissue deformation), chemical (e.g. exposure to acid or irritant), or thermal (e.g. high or low temperatures).

There are some types of tissue damage that are not detected by any sensory receptors, and thus cannot cause pain. Therefore, not all noxious stimuli are adequate stimuli of nociceptors. The adequate stimuli of nociceptors are termed nociceptive stimuli. A nociceptive stimulus is defined as "an actually or potentially tissue damaging event transduced and encoded by nociceptors."^[1]

References

^ ^a ^b ^c Loeser JD, Treede RD. (2008). "The Kyoto protocol of IASP Basic Pain Terminology.". Pain 137 (3): 473–7. doi:10.1016/j.pain.2008.04.025. PMID 18583048.

UpToDate Contents

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1. 小児における傾眠および昏睡の評価 evaluation of stupor and coma in children
2. 低酸素性虚血性脳障害：評価および予後 hypoxic ischemic brain injury evaluation and prognosis
3. 慢性疼痛の定義および病因 definition and pathogenesis of chronic pain
4. 新生児疼痛の評価 assessment of neonatal pain
5. 新生児の神経学的検査 neurological examination of the newborn

English Journal

Extreme thermal noxious stimuli induce pain responses in zebrafish larvae.

Malafoglia V, Colasanti M, Raffaeli W, Balciunas D, Giordano A, Bellipanni G.Author information Sbarro Institute for Cancer Research and Molecular Medicine, Temple University, Philadelphia, Pennsylvania; ISAL-Foundation, Institute for Research on Pain, Torre Pedrera (RN), Italy.AbstractExposing tissues to extreme high or low temperature leads to burns. Burned animals sustain several types of damage, from the disruption of the tissue to degeneration of axons projecting through muscle and skin. Such damage causes pain due to both inflammation and axonal degeneration (neuropathic-like pain). Thus, the approach to cure and alleviate the symptoms of burns must be twofold: rebuilding the tissue that has been destroyed and alleviating the pain derived from the burns. While tissue regeneration techniques have been developed, less is known on the treatment of the induced pain. Thus, appropriate animal models are necessary for the development of the best treatment for pain induced in burned tissues. We have developed a methodology in the zebrafish aimed to produce a new animal model for the study of pain induced by burns. Here, we show that two events linked to the onset of burn-induced inflammation and neuropathic-like pain in mammals, degeneration of axons innervating the affected tissues and over-expression of specific genes in sensory tissues, are conserved from zebrafish to mammals.
Journal of cellular physiology.J Cell Physiol.2014 Mar;229(3):300-8. doi: 10.1002/jcp.24447.
Exposing tissues to extreme high or low temperature leads to burns. Burned animals sustain several types of damage, from the disruption of the tissue to degeneration of axons projecting through muscle and skin. Such damage causes pain due to both inflammation and axonal degeneration (neuropathic-lik
PMID 23929528

Cortistatin attenuates inflammatory pain via spinal and peripheral actions.

Morell M1, Camprubí-Robles M2, Culler MD3, de Lecea L4, Delgado M5.Author information 1Institute of Parasitology and Biomedicine Lopez-Neyra, IPBLN-CSIC, 18016 Granada, Spain.2Institute of Molecular and Cell Biology, Miguel Hernandez University, 03202 Alicante, Spain.3IPSEN Group, Milford, MA 01757, USA.4Department of Psychiatry and Behavioral Sciences, Stanford University, Stanford, CA 94305, USA.5Institute of Parasitology and Biomedicine Lopez-Neyra, IPBLN-CSIC, 18016 Granada, Spain. Electronic address: mdelgado@ipb.csic.es.AbstractClinical pain, as a consequence of inflammation or injury of peripheral organs (inflammatory pain) or nerve injury (neuropathic pain), represents a serious public health issue. Treatment of pain-related suffering requires knowledge of how pain signals are initially interpreted and subsequently transmitted and perpetuated. To limit duration and intensity of pain, inhibitory signals participate in pain perception. Cortistatin is a cyclic-neuropeptide that exerts potent inhibitory actions on cortical neurons and immune cells. Here, we found that cortistatin is a natural analgesic component of the peripheral nociceptive system produced by peptidergic nociceptive neurons of the dorsal root ganglia in response to inflammatory and noxious stimuli. Moreover, cortistatin is produced by GABAergic interneurons of deep layers of dorsal horn of spinal cord. By using cortistatin-deficient mice, we demonstrated that endogenous cortistatin critically tunes pain perception in physiological and pathological states. Furthermore, peripheral and spinal injection of cortistatin potently reduced nocifensive behavior, heat hyperalgesia and tactile allodynia in experimental models of clinical pain evoked by chronic inflammation, surgery and arthritis. The analgesic effects of cortistatin were independent of its anti-inflammatory activity and directly exerted on peripheral and central nociceptive terminals via Gαi-coupled somatostatin-receptors (mainly sstr2) and blocking intracellular signaling that drives neuronal plasticity including protein kinase A-, calcium- and Akt/ERK-mediated release of nociceptive peptides. Moreover, cortistatin could modulate, through its binding to ghrelin-receptor (GHSR1), pain-induced sensitization of secondary neurons in spinal cord. Therefore, cortistatin emerges as an anti-inflammatory factor with potent analgesic effects that offers a new approach to clinical pain therapy, especially in inflammatory states.
Neurobiology of disease.Neurobiol Dis.2014 Mar;63:141-54. doi: 10.1016/j.nbd.2013.11.022. Epub 2013 Dec 9.
Clinical pain, as a consequence of inflammation or injury of peripheral organs (inflammatory pain) or nerve injury (neuropathic pain), represents a serious public health issue. Treatment of pain-related suffering requires knowledge of how pain signals are initially interpreted and subsequently trans
PMID 24333694

Altered nociceptive, endocrine, and dorsal horn neuron responses in rats following a neonatal immune challenge.

Zouikr I1, Tadros MA2, Barouei J1, Beagley KW3, Clifton VL4, Callister RJ2, Hodgson DM5.Author information 1Laboratory of Neuroimmunology, School of Psychology, University of Newcastle, Newcastle, New South Wales, Australia.2School of Biomedical Sciences and Pharmacy, University of Newcastle, Newcastle, New South Wales, Australia.3Institute of Health Biomedical Innovation, Queensland University of Technology, Brisbane, Queensland, Australia.4Robinson Institute, University of Adelaide, Adelaide, South Australia, Australia.5Laboratory of Neuroimmunology, School of Psychology, University of Newcastle, Newcastle, New South Wales, Australia. Electronic address: Deborah.Hodgson@newcastle.edu.au.AbstractThe neonatal period is characterized by significant plasticity where the immune, endocrine, and nociceptive systems undergo fine-tuning and maturation. Painful experiences during this period can result in long-term alterations in the neurocircuitry underlying nociception, including increased sensitivity to mechanical or thermal stimuli. Less is known about the impact of neonatal exposure to mild inflammatory stimuli, such as lipopolysaccharide (LPS), on subsequent inflammatory pain responses. Here we examine the impact of neonatal LPS exposure on inflammatory pain sensitivity and HPA axis activity during the first three postnatal weeks. Wistar rats were injected with LPS (0.05mg/kg IP, Salmonella enteritidis) or saline on postnatal days (PNDs) 3 and 5 and later subjected to the formalin test at PNDs 7, 13, and 22. One hour after formalin injection, blood was collected to assess corticosterone responses. Transverse spinal cord slices were also prepared for whole-cell patch clamp recording from lumbar superficial dorsal horn neurons (SDH). Brains were obtained at PND 22 and the hypothalamus was isolated to measure glucocorticoid (GR) and mineralocorticoid receptor (MR) transcript expression using qRT-PCR. Behavioural analyses indicate that at PND 7, no significant differences were observed between saline- or LPS-challenged rats. At PND 13, LPS-challenged rats exhibited enhanced licking (p<.01), and at PND 22, increased flinching in response to formalin injection (p<.05). LPS-challenged rats also displayed increased plasma corticosterone at PND 7 and PND 22 (p<.001) but not at PND 13 following formalin administration. Furthermore, at PND 22 neonatal LPS exposure induced decreased levels of GR mRNA and increased levels of MR mRNA in the hypothalamus. The intrinsic properties of SDH neurons were similar at PND 7 and PND 13. However, at PND 22, ipsilateral SDH neurons in LPS-challenged rats had a lower input resistance compared to their saline-challenged counterparts (p<.05). These data suggest neonatal LPS exposure produces developmentally regulated changes in formalin-induced behavioural responses, corticosterone levels, and dorsal horn neuron properties following noxious stimulation later in life. These findings highlight the importance of immune activation during the neonatal period in shaping pain sensitivity later in life. This programming involves both spinal cord neurons and the HPA axis.
Psychoneuroendocrinology.Psychoneuroendocrinology.2014 Mar;41:1-12. doi: 10.1016/j.psyneuen.2013.11.016. Epub 2013 Dec 4.
The neonatal period is characterized by significant plasticity where the immune, endocrine, and nociceptive systems undergo fine-tuning and maturation. Painful experiences during this period can result in long-term alterations in the neurocircuitry underlying nociception, including increased sensiti
PMID 24495603

Japanese Journal

Pain Perception and Anaesthesia in Research Frogs

GUÉNETTE Sarah Annie,GIROUX Marie-Chantal,VACHON Pascal
Experimental Animals 62(2), 87-92, 2013
… Frogs possess pain receptors and pathways that support processing and perception of noxious stimuli however the level of organization is less well structured compared to mammals. …
NAID 130003362950

The Orally Administered Selective TRPV1 Antagonist, JTS653, Attenuates Chronic Pain Refractory to Non-steroidal Anti-inflammatory Drugs in Rats and Mice Including Post-herpetic Pain

Kitagawa Yoshihiro,Tamai Isao,Hamada Yuji,Usui Kenji,Wada Masashi,Sakata Masahiro,Matsushita Mutsuyoshi
Journal of Pharmacological Sciences, 2013
… JTS-653 did not affect the nociception of noxious thermal and mechanical stimuli and motor coordination in normal rats. …
NAID 130003362708

Changes in Response Behaviors to Noxious Heat and Mechanical Stimuli After Carrageenan-induced Inflammation in Mice Treated with Capsaicin 2 or 15 days After Birth

Hiura Akio,Nakagawa H,樋浦明夫
WebmedCentral NEUROSCIENCES, 2012-12-06
… The aim of the present study was to investigate thecause of normal response behaviors to noxious heatdespite the marked loss of small neurons in the dorsalroot ganglion (DRG) as a result of neonatal capsaicintreatment. …
NAID 120005037543