Wikidata:WikiProject Chronic Pain/Biology

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Interesting summaries and lists edit

Neurotransmitter (w, wd, sub) edit

Neuropeptide (w, wd, sub) edit

  • Substance P (w, wd, src) Is released from the terminals of specific sensory nerves. When pain is perceived, pain receptors (nociceptors) send signals to the dorsal horn of the spinal cord and then up to the hypothalamus through the release of a neuropeptide called substance P.[1] Amplifies or excites most cellular processes. Stimulate IL-6 and TNF release from mast cells. Initiates expression of almost all known immunological chemical messengers (cytokines). Found in higher doses in serum of patients with Fibromyalgia.
  • Oxytocin (w, wd, src)
  • beta-endorphin (w, wd, src)

Amino acid (w, wd, sub) edit

Monoamine neurotransmitter (w, wd, sub) edit

Gaseous signaling molecules (w, wd, sub) edit

Trace amine (w, wd, sub) edit

Purinergic signalling (w, wd, sub) edit

Other neurotransmiters edit

hormone (w, wd, sub) edit

Amino acid (w, wd, sub) edit

Peptide (w, wd, sub) edit

  • Vasopressin (w, wd, src)
  • Corticotropin-releasing hormone (w, wd, src) Hormone related with stress response, parturition and inflamation. Stimulate IL-6 and TNF release from mast cells. Found in higher doses of serums of patients with Fibromyalgia.
  • Leptin (w, wd, src) A hormone predominantly made by adipose cells that helps to regulate energy balance by inhibiting hunger. In obesity, a decreased sensitivity to leptin occurs. Is a potent microglia cell primer.

Protein (w, wd, sub) edit

Glycoprotein (w, wd, sub) edit

Eicosanoid (w, wd, sub) edit

Steroid (w, wd, sub) edit

Cells edit

Neuroglia (w, wd, src) edit

white blood cell (w, wd, src) edit

  • mast cells (w, wd, src) Mast cells are involved in FM by releasing proinflammatory cytokines, chemokines, chemical mediators, and PGD2. TNF is a cytokine generated by MCs and its level is higher in FM. [4]

Interleukin (w, wd, src) edit

Lymphokine (w, wd, src) edit

Monokine (w, wd, src) edit

interferon (w, wd, src) edit

Cytokine_receptor (w, wd, src) edit

Opioid System edit

  • Opioid (w, wd, src)
    • Morphine (w, wd, src)
    • Endogeous opioids
      • Dynorphin (w, wd, src) Dynorphin produced in magnocellular oxytocin neurons is a negative feedback inhibitor of oxytocin secretion. Dynorphin produced in the arcuate nucleus and in orexin neurons of the lateral hypothalamus affects the control of appetite. 6-10 times more potent than morphine on a per mole basis.
      • Enkephalin (w, wd, src) During a stress response, several Met-enkephalin analogs had increased activity in the hippocampus, while Leu-enkephalin analogs as well as somatostatins were downregulated during stress.
      • Endorphin (w, wd, src) The principal function of endorphins is to inhibit the communication of pain signals; they may also produce a feeling of euphoria very similar to that produced by other opioids.
        • Alpha-endorphin (w, wd, src)
        • Beta-endorphin (w, wd, src) β-Endorphin has been primarily studied for its influence on nociception (i.e., pain perception). β-endorphin modulates pain perception both in the central nervous system and the peripheral nervous system. In the peripheral nervous system, T-lymphocytes release β-endorphin in this localized region, allowing it to bind to opioid receptors, causing direct inhibition of substance P. In the central nervous system, β-endorphin binds to opioid receptors in the dorsal root and inhibits the release of substance P in the spinal cord. The hypothalamus responds to the pain signal by releasing β-endorphin through the periaqueductal grey network, which mainly acts to inhibit the release of GABA, a neurotransmitter which prevents the release of dopamine.
        • Gamma-endorphin (w, wd, src)
      • Endomorphins (w, wd, src)
      • Nociceptin (w, wd, src) blocking the nociceptin receptor can lead to an increased pain threshold and a decreased tolerance development to analgesic opioids
  • Opioid receptor (w, wd, src)
    • κ-opioid receptor (w, wd, src) Binds the opioid peptide dynorphin as the primary endogenous ligand. There is evidence that distribution and/or function of this receptor may differ between sexes. KOR agonists are potently analgesic, and have been employed clinically in the treatment of pain. However, KOR agonists also produce side effects such as dysphoria, hallucinations, and dissociation, which has limited their clinical usefulness.
    • mu opioid receptors (w, wd, src) Possibly less available in patients with Fibromylagia [5]
  • Cannabinoid receptor (w, wd, src)
    • Cannabinoid receptor type 1 (w, wd, src) Is expressed in the peripheral nervous system and central nervous system. Induces a reduction in GABA-mediated neurotransmission. Modulate neurotransmitter release in a manner that prevents the development of excessive neuronal activity, reducing pain and other inflammatory symptoms. Activation of peripheral CB1 receptors contributes to hemorrhagic and endotoxin-induced hypotension.
    • Cannabinoid receptor type 2 (w, wd, src) CB2 receptors are mainly expressed on T cells of the immune system, on macrophages and B cells, and in hematopoietic cells. They also have a function in keratinocytes. They are also expressed on peripheral nerve terminals. These receptors play a role in antinociception, or the relief of pain. In the brain, they are mainly expressed by microglial cells, where their role remains unclear. Later studies examining the effect of synthetic cannabinoid agonist JWH-015 on CB2 receptors revealed that changes in cAMP levels result in the phosphorylation of leukocyte receptor tyrosine kinase at Tyr-505, leading to an inhibition of T cell receptor signaling. Thus, CB2 agonists may also be useful for treatment of inflammation and pain, and are currently being investigated, in particular for forms of pain that do not respond well to conventional treatments, such as neuropathic pain.[40] Consistent with these findings are studies that demonstrate increased CB2 receptor expression in the spinal cord, dorsal root ganglion, and activated microglia in the rodent neuropathic pain model, as well as on human heptocellular carcinoma tumor samples.
    • NAGly receptor (w, wd, src)
    • GPR55 (w, wd, src)
    • GPR119 (w, wd, src)

Adrenergic receptor (w, wd, src) edit

Imidazoline (w, wd, src) edit

  • Imidazoline receptor (w, wd, src) There are three main classes of imidazoline receptor: I1 is involved in inhibition of the sympathetic nervous system to lower blood pressure, I2 has as yet uncertain functions but is implicated in several psychiatric conditions, and I3 regulates insulin secretion. Preliminary research in rodents suggests that I2 receptor agonists may be effective in chronic, but not acute pain, including fibromyalgia.
  • 2-imidazoline (w, wd, src) 2-imidazolines have been investigated as antihyperglycemic, anti-inflammatory, antihypertensive, antihypercholesterolemic, and antidepressant reagents.[1][5] The imidazoline-containing drug clonidine is used alone or in combination with other medications to treat high blood pressure. It is also used in the treatment of dysmenorrhea, hypertensive crisis, Tourette's syndrome and attention deficit hyperactivity disorder (ADHD). Studies suggest that I2 imidazoline compounds can partially or fully agonize D2DR (D2-dopamine receptors) with a strength similar to dopamine.

Others edit

  • HK1 (w, wd, src) Enzyme related to the metabolism of Glucose and neurotransmission. Found in higher levels in serum from patients with Fibromyalgia.
  • Adénosine triphosphate (w, wd, src) Microglias of Fibro patients may react more to ATP.
  • glucose (w, wd, src) Form of sugar. Potent microglia cell primer.

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== Articles lists ==

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*[https://query.wikidata.org/#SELECT%20DISTINCT%20%3Fitem%20%3FitemLabel%20%3Fpublication_date%20%3FDOI%20%0AWHERE%20%7B%0A%20%20hint%3AQuery%20hint%3Aoptimizer%20%22None%22.%0A%20%20SERVICE%20wikibase%3Amwapi%20%7B%0A%20%20%20%20bd%3AserviceParam%20wikibase%3Aapi%20%22Search%22%3B%0A%20%20%20%20%20%20%20%20%20%20%20%20%20%20%20%20%20%20%20%20wikibase%3Aendpoint%20%22www.wikidata.org%22%3B%0A%20%20%20%20%20%20%20%20%20%20%20%20%20%20%20%20%20%20%20%20mwapi%3Asrsearch%20%22keyword%20pain%20haswbstatement%3AP31%3DQ13442814%22.%0A%20%20%20%20%3Ftitle%20wikibase%3AapiOutput%20mwapi%3Atitle.%0A%20%20%7D%0A%20%20BIND%28IRI%28CONCAT%28STR%28wd%3A%29%2C%20%3Ftitle%29%29%20AS%20%3Fitem%29%0A%20%20SERVICE%20wikibase%3Alabel%20%7B%20bd%3AserviceParam%20wikibase%3Alanguage%20%22%5BAUTO_LANGUAGE%5D%2Cen%22.%20%7D%0A%20%20OPTIONAL%20%7B%20%3Fitem%20wdt%3AP577%20%3Fpublication_date.%20%7D%0A%20%20OPTIONAL%20%7B%20%3Fitem%20wdt%3AP356%20%3FDOID.%20%7D%0A%20%20BIND%28URI%28CONCAT%28STR%28%22https%3A%2F%2Fdx.doi.org%2F%22%29%2C%20%3FDOID%29%29%20AS%20%3FDOI%29%0A%7D%0AORDER%20BY%20DESC%28%3Fpublication_date%29%20 List of articles] with {{Q|Qid_main}} and "pain" in the title, most recents first. (always up to date)
*[https://query.wikidata.org/#SELECT%20%3Fitem%20%3FitemLabel%20%3Fpublication_date%20%3FDOI%20WHERE%20%7B%0A%20%20%3Fitem%20wdt%3AP921%20wd%3AQid_main.%0A%20%20SERVICE%20wikibase%3Alabel%20%7B%20bd%3AserviceParam%20wikibase%3Alanguage%20%22%5BAUTO_LANGUAGE%5D%2Cen%22.%20%7D%0A%20%20OPTIONAL%20%7B%20%3Fitem%20wdt%3AP577%20%3Fpublication_date.%20%7D%0A%20%20OPTIONAL%20%7B%20%3Fitem%20wdt%3AP356%20%3FDOID.%20%7D%0A%20%20BIND%28URI%28CONCAT%28STR%28%22https%3A%2F%2Fdx.doi.org%2F%22%29%2C%20%3FDOID%29%29%20AS%20%3FDOI%29%0A%7D%0AORDER%20BY%20DESC%28%3Fpublication_date%29%20 List of articles] with {{P|P921}} settled to {{Q|Qid_main}}, most recents first. (may include other articles)

== Reading list ==

{{List of scholarly articles/Header}}
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== Articles related to chronic pain ==

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References edit

  1. w:Beta-Endorphin
  2. New challenges in the study of the mammalian tachykinins
  3. TAC1 tachykinin precursor 1 on NCBI
  4. Low-grade chronic inflammation mediated by mast cells in fibromyalgia: role of IL-37.
  5. Decreased central mu-opioid receptor availability in fibromyalgia.
  6. Microglial GRK2: A novel regulator of transition from acute to chronic pain