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Related Concept Videos

Nociception01:44

Nociception

33.5K
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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Sensory Functions of the Skin01:16

Sensory Functions of the Skin

8.9K
The skin is the largest organ of the human body and plays a crucial role in our sensory perception. It contains a vast network of sensory receptors that contribute to the skin's protective function by perceiving physical, biological, and environmental cues and generating relevant responses.
There are two main categories of receptors on the skin: capsulated and non-capsulated. The non-capsulated ones are mainly the pain receptors. The capsulated ones can be further categorized based on the...
8.9K
Local Anesthetics: Differential Sensitivity of Nerve Fibers01:24

Local Anesthetics: Differential Sensitivity of Nerve Fibers

1.5K
Local anesthetics (LAs) block the sodium channels of nerve trunks, sensory nerve endings, and neuromuscular junctions. Although LAs can block all kinds of nerves, the sensitivity of nerve fibers differs according to nerve types and structures. LAs are known to block myelinated fibers faster than unmyelinated ones. Also, they block pain or sensory neurons at low concentrations without affecting the motor neurons involved in muscle contractions. This helps relieve labor pain without affecting the...
1.5K
Pain01:20

Pain

1.6K
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...
1.6K
Integration of Synaptic Events01:28

Integration of Synaptic Events

5.0K
Synaptic integration mainly includes the summation of graded potentials. Graded potentials, regardless of their type, cause subtle alterations in membrane voltage, resulting in either depolarization or hyperpolarization. These incremental changes, when combined or summed, can propel the neuron toward its threshold. Consider, for example, a membrane experiencing a +15 mV shift, causing it to depolarize from -70 mV to -55 mV. In this scenario, graded potentials govern the membrane's ability to...
5.0K
Analgesia and Pain Management01:25

Analgesia and Pain Management

2.4K
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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Related Experiment Video

Updated: Mar 1, 2026

Advanced Glycation End-Products Sensitize Human Sensory-Like Neuron Cells to Capsaicin-Induced Calcium Influx
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Advanced Glycation End-Products Sensitize Human Sensory-Like Neuron Cells to Capsaicin-Induced Calcium Influx

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Epac and Nociceptor Sensitization.

Li-Yen Huang, Yanping Gu1

  • 1Department of Neuroscience and Cell Biology, University of Texas Medical Branch Galveston, TX 77555-1069, USA.

Molecular Pain
|June 6, 2017
PubMed
Summary

Inflammation causes sensory neurons to overreact, leading to chronic pain. New research shows cyclic adenosine monophosphate (cAMP) and exchange proteins activated by cAMP (Epacs) signaling contribute to this pain hypersensitivity.

Area of Science:

  • Neuroscience
  • Pain Research
  • Molecular Biology

Background:

  • Primary sensory neurons transmit sensory input to the central nervous system.
  • Inflammation enhances and prolongs neuronal responses, causing chronic pain.
  • Prostaglandin E2 (PGE2) is a key inflammatory mediator in abnormal pain responses.

Purpose of the Study:

  • To review the role of cyclic adenosine monophosphate (cAMP) and exchange proteins activated by cAMP (Epacs) signaling in pain hypersensitivity.
  • To elucidate the mechanisms by which PGE2-induced cAMP activates Epacs after inflammation.
  • To understand the contribution of cAMP-Epac signaling to exaggerated nociceptive responses.

Main Methods:

  • Review of existing scientific literature on sensory neurons, inflammation, and pain signaling pathways.

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Chronic Post-Ischemia Pain Model for Complex Regional Pain Syndrome Type-I in Rats
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Advanced Glycation End-Products Sensitize Human Sensory-Like Neuron Cells to Capsaicin-Induced Calcium Influx
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Tissue Preparation and Immunostaining of Mouse Sensory Nerve Fibers Innervating Skin and Limb Bones
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Chronic Post-Ischemia Pain Model for Complex Regional Pain Syndrome Type-I in Rats

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  • Analysis of molecular mechanisms involving prostaglandin E2 (PGE2), G protein-coupled EP receptors, adenylyl cyclase, and cAMP.
  • Examination of the differential activation of protein kinase A and Epacs by cAMP under inflammatory conditions.

    • Main Results:

    • PGE2 activates adenylyl cyclase, increasing intracellular cAMP levels.
    • Following inflammation, cAMP activates both protein kinase A and Epacs.
    • Epac activation by cAMP contributes to PGE2-mediated hyperalgesia and pain hypersensitivity.

    Conclusions:

    • The cAMP-Epac signaling pathway plays a significant role in the development of inflammatory pain hypersensitivity.
    • Targeting the cAMP-Epac pathway may offer novel therapeutic strategies for chronic pain management.
    • Understanding these molecular mechanisms is crucial for advancing pain research.