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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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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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Somatosensation01:33

Somatosensation

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The somatosensory system relays sensory information from the skin, mucous membranes, limbs, and joints. Somatosensation is more familiarly known as the sense of touch. A typical somatosensory pathway includes three types of long neurons: primary, secondary, and tertiary. Primary neurons have cell bodies located near the spinal cord in groups of neurons called dorsal root ganglia. The sensory neurons of ganglia innervate designated areas of skin called dermatomes.
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Integration of Synaptic Events01:28

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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...
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Neuroplasticity01:01

Neuroplasticity

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Neuroplasticity reflects the brain's remarkable capacity to adapt and evolve, responding dynamically to learning, experiences, or injury by reorganizing its neural circuitry. This reorganization involves creating new neural connections and refining old ones through a series of biological processes that contribute to the brain's lifelong development and adaptability.
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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: Aug 22, 2025

The Sciatic Nerve Cuffing Model of Neuropathic Pain in Mice
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Synaptic Plasticity in the Pain-Related Cingulate and Insular Cortex.

Jung-Hyun Alex Lee1, Qiyu Chen2,3, Min Zhuo1,2,4

  • 1Department of Physiology, Faculty of Medicine, University of Toronto, Medical Science Building, 1 King's College Circle, Toronto, ON M5S 1A8, Canada.

Biomedicines
|November 11, 2022
PubMed
Summary

Chronic pain involves the anterior cingulate cortex (ACC) and insular cortex (IC). Inhibiting synaptic plasticity, like long-term potentiation (LTP), in these brain regions may reduce pain and emotional changes.

Keywords:
anterior cingulate cortexchronic painlong-term potentiationneuropathic painsynaptic plasticity

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Area of Science:

  • Neuroscience
  • Pain Research
  • Synaptic Plasticity

Background:

  • The anterior cingulate cortex (ACC) and insular cortex (IC) are key brain regions for pain perception and chronic pain.
  • Neuronal synapses in these areas exhibit plasticity, including long-term potentiation (LTP), similar to learning and memory centers.

Purpose of the Study:

  • To review recent advancements in understanding cortical long-term potentiation (LTP) mechanisms.
  • To explore the contribution of cortical LTP to behavioral pain and emotional alterations.

Main Methods:

  • Summary of genetic and pharmacological studies.
  • Review of research on synaptic mechanisms of cortical LTP.

Main Results:

  • Inhibiting cortical LTP can decrease injury-induced behavioral sensitization.
  • Cortical LTP inhibition may also alleviate injury-induced emotional changes.

Conclusions:

  • Cortical LTP is a significant factor in pain perception and chronic pain development.
  • Targeting cortical synaptic plasticity offers a potential therapeutic strategy for pain and associated emotional disorders.