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Nociception01:44

Nociception

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Nociception—the ability to feel pain—is essential for an organism’s survival and overall well-being. Noxious stimuli such as piercing pain from a sharp object, heat from an open flame, or contact with corrosive chemicals are first detected by sensory receptors, called nociceptors, located on nerve endings. Nociceptors express ion channels that convert noxious stimuli into electrical signals. When these signals reach the brain via sensory neurons, they are perceived as pain.
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Analgesia and Pain Management01:25

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Pain is critical to various clinical pathologies, provoking an urgent need for effective management. Pain, whether acute or chronic, is a complex neurochemical process. Its alleviation depends on the type, with nonopioid analgesics effective for mild to moderate pain, such as musculoskeletal or inflammatory pain, while neuropathic pain responds best to anticonvulsants, tricyclic antidepressants, or serotonin/norepinephrine reuptake inhibitors. For severe acute or chronic pain, opioids may be...
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Pain01:20

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Pain serves as a critical warning signal that alerts the body to potential or actual harm. When mechanical pressure on the skin is intense, such as from a sharp pinch, the sensation transitions from touch to pain. Similarly, extreme temperatures, like a hot pot handle, convert the sensation of heat into pain. Pain can also result from overstimulation of other senses, such as blinding light, loud noise, or the intense heat from habañero peppers. This ability to sense pain is essential for...
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Opioid Receptors: Overview01:22

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Opioid receptors, including the mu (μ, MOR), delta (δ, DOR), and kappa (κ, KOR) types, belong to the rhodopsin family of G protein-coupled receptors. These receptors are located throughout the central and peripheral nervous systems and in non-neuronal tissues such as macrophages and astrocytes. Opioid receptor ligands can be categorized into agonists or antagonists. Highly selective agonists include [d-Ala2, MePhe4, Gly(ol)5]-enkephalin or DAMGO for MOR, [D-Pen2,...
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Nitric Oxide Signaling Pathway01:28

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Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure...
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Ganglionic stimulants activate NM nicotinic receptors in autonomic ganglia, falling into two categories: nicotine mimetics [e.g., lobeline, dimethylpiperazine, tetramethylammonium] and muscarinic receptor agonists [e.g., muscarine, methacholine]. The first category's action is rapid and blocked by nicotinic receptor antagonists, while the second category's action is delayed and blocked by atropine-like agents. Nicotine, an alkaloid, affects the heart rate by stimulating...
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GnRH peripherally modulates nociceptor functions, exacerbating mechanical pain.

Haiyan Zheng1, Minseok Kim1, Chaeun Kim1

  • 1Department of Biomedical Sciences, Korea University College of Medicine, Seoul, Republic of Korea.

Frontiers in Molecular Neuroscience
|May 24, 2024
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Summary

Gonadotropin-releasing hormone (GnRH) aggravates pain by acting on peripheral pain-sensing neurons (nociceptors) in mice. This neurohormone enhances pain signaling, suggesting a novel peripheral mechanism for pain modulation.

Keywords:
DRG neuronGNRHRGnRHneuropathic painpain

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Area of Science:

  • Neuroscience
  • Pain Research
  • Endocrinology

Background:

  • Peripheral nociceptors transmit pain signals to the brain.
  • Neurohormonal substances modulate nociceptor function.
  • The role of gonadotropin-releasing hormone (GnRH) in peripheral pain modulation is not fully understood.

Purpose of the Study:

  • To investigate the role of gonadotropin-releasing hormone (GnRH) in modulating peripheral nociceptor activity.
  • To determine if GnRH influences pain perception via peripheral mechanisms.

Main Methods:

  • Investigated the expression of GnRH and its receptor (GnRHR) in mouse nociceptors.
  • Administered GnRH and its analogue to mice to assess effects on mechanical pain.
  • Examined GnRH effects on nociceptor function in vitro, including involvement of transient receptor potential (TRP) channels.

Main Results:

  • GnRH and GnRHR were found in a subpopulation of peripheral nociceptors.
  • Peripheral administration of GnRH exacerbated mechanical pain in mice, including in neuropathic models.
  • GnRH treatment promoted nociceptor activity in vitro, involving specific sensory TRP channels.

Conclusions:

  • Peripheral GnRH positively modulates nociceptor activity in a receptor-dependent manner.
  • GnRH contributes to pain exacerbation through a peripheral mechanism.
  • This study highlights GnRH's significant role in neurohormonal pain modulation.