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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. Thus, pain helps the...
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Related Experiment Video

Updated: Jul 7, 2026

Tissue Preparation and Immunostaining of Mouse Sensory Nerve Fibers Innervating Skin and Limb Bones
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Decrease of growth and differentiation factor 10 contributes to neuropathic pain through N-methyl-D-aspartate

Long Jiang1, Botao Tan, Sen Li

  • 1aState Key of Laboratory of Trauma, Burns and Combined Injury, Institute of Surgery Research, Daping Hospital, Third Military Medical University bDepartment of Rehabilitation Medicine, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.

Neuroreport
|April 11, 2017
PubMed
Summary

Decreased growth and differentiation factor 10 (GDF10) expression is linked to neuropathic pain. Blocking N-methyl-D-aspartate (NMDA) receptors reduces pain and normalizes GDF10 levels, suggesting GDF10

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Area of Science:

  • Neuroscience
  • Pain Research
  • Molecular Biology

Background:

  • Neuropathic pain is a chronic condition characterized by allodynia and hyperalgesia.
  • The transforming growth factor-β superfamily has demonstrated protective effects against neuropathic pain.

Purpose of the Study:

  • To investigate the role of growth and differentiation factor 10 (GDF10) in neuropathic pain.
  • To explore the relationship between GDF10 expression, N-methyl-D-aspartate (NMDA) receptor activation, and pain sensitivity.

Main Methods:

  • Investigated GDF10 expression in spinal dorsal horn neurons.
  • Utilized spinal nerve ligation and NMDA intrathecal infusion models.
  • Administered MK-801, an NMDA receptor antagonist, to assess its effects on GDF10 and pain.

Main Results:

  • GDF10 is primarily expressed in superficial spinal dorsal horn neurons.
  • GDF10 expression was significantly downregulated following spinal nerve ligation and NMDA infusion.
  • Reduced GDF10 levels correlated with increased mechanical sensitivity.
  • MK-801 treatment prevented the decrease in GDF10 and the rise in mechanical sensitivity.

Conclusions:

  • Decreased GDF10 expression may contribute to neuropathic pain development.
  • GDF10 downregulation appears to be linked to NMDA receptor activation.
  • These findings offer insights into the molecular mechanisms of neuropathic pain.