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Related Concept Videos

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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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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Adrenergic Receptors: ɑ Subtype01:31

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Adrenoceptors are classified into α and ꞵ classes based on their potencies to catecholamine agonists. α-adrenoceptors show the following order of catecholamine potency:
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Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

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Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
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Acute Inflammation II: Local and Systemic Effects01:25

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Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...
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Thermosensation01:43

Thermosensation

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Peripheral thermosensation is the perception of external temperature. A change in temperature (on the surface of the skin and other tissues) is detected by a family of temperature-sensitive ion channels called Transient Receptor Potential, or TRP, receptors. These receptors are located on free nerve endings. Those detecting cold temperatures are closer to the surface of the skin than the nerve endings detecting warmth. These thermoTRP channels, while temperature selective, have relatively...
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Related Experiment Video

Updated: Apr 21, 2026

A Simple and Inexpensive Method for Determining Cold Sensitivity and Adaptation in Mice
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Annexin A2 regulates TRPA1-dependent nociception.

Luca Avenali1, Pratibha Narayanan1, Tom Rouwette1

  • 1Somatosensory Signalling Group and.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|October 31, 2014
PubMed
Summary

Annexin A2 (AnxA2) limits the availability of transient receptor potential A1 (TRPA1) channels. AnxA2 deficiency enhances TRPA1-mediated pain signaling and nocifensive behaviors in vertebrates.

Keywords:
TRPA1 channelsmembrane abundancenociceptionprotein–protein interaction

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pain Research

Background:

  • The molecular mechanisms regulating transient receptor potential A1 (TRPA1) channels, crucial for vertebrate pain sensation, remain incompletely understood.
  • While TRPA1 activation is well-studied, the proteins that control its function and localization are largely unknown.

Purpose of the Study:

  • To identify novel molecular regulators of TRPA1 channel function using a proteomics-based approach.
  • To investigate the role of Annexin A2 (AnxA2) in the regulation of TRPA1 in sensory neurons and its impact on pain signaling.

Main Methods:

  • Unbiased proteomics to identify TRPA1-interacting proteins in mouse sensory neurons.
  • Immunofluorescence to assess AnxA2 and TRPA1 co-localization.
  • Analysis of TRPA1 membrane levels in AnxA2-deficient (AnxA2-/-) mouse sensory neurons.
  • Calcium imaging to measure TRPA1 channel activity in cultured neurons.
  • In vivo behavioral assays to evaluate pain responses in AnxA2-/- mice.

Main Results:

  • Annexin A2 (AnxA2) was identified as a binding partner of native TRPA1 channels in mouse sensory neurons.
  • AnxA2 is expressed in a subset of TRPA1-positive sensory neurons.
  • AnxA2 deficiency leads to increased TRPA1 membrane expression and heightened neuronal responsiveness to TRPA1 agonists.
  • AnxA2 knockout mice exhibit exaggerated TRPA1-dependent acute and inflammatory pain behaviors, while TRPV1-mediated pain and other sensory modalities remain unaffected.

Conclusions:

  • Annexin A2 (AnxA2) physically associates with TRPA1 channels and negatively regulates their surface expression.
  • AnxA2 acts as a key molecular brake on TRPA1 availability, thereby modulating nociceptive signaling.
  • Targeting the AnxA2-TRPA1 interaction may offer novel therapeutic strategies for managing TRPA1-mediated pain conditions.