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Related Concept Videos

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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Plasticity00:58

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Plasticity is the property where an object loses its elasticity and undergoes irreversible deformation, even after the deformation forces are eliminated. If a material deforms irreversibly without increasing stress or load, then this is called ideal plasticity. For example, when a force is applied to an aluminum rod, it changes its shape, but it does not return to its original shape once the force is removed. Plastic deformation or ductility is thus a permanent deformation or change in the...
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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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Local Anesthetics: Differential Sensitivity of Nerve Fibers01:24

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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...
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Long-term Potentiation01:25

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Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
Hebbian LTP
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Overview of Somatic Sensory Pathways01:29

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Somatic sensory or somatosensory pathways refer to the neural pathways that carry information related to touch, pressure, pain, temperature, and proprioception from the skin, muscles, tendons, and joints to the brain. These pathways involve several stages of processing and integration of sensory information.
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Related Experiment Video

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Inducing Long-Term Plasticity of Intrinsic Neuronal Excitability in Neurons of the Dorsal Lateral Geniculate Nucleus
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Inducing Long-Term Plasticity of Intrinsic Neuronal Excitability in Neurons of the Dorsal Lateral Geniculate Nucleus

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Nociceptor plasticity: A closer look.

Maria Caterina Pace1, Maria Beatrice Passavanti1, Lorenzo De Nardis1

  • 1Department of Anaesthesiological, Surgical and Emergency Sciences, Second University of Naples, Naples, Italy.

Journal of Cellular Physiology
|May 11, 2017
PubMed
Summary
This summary is machine-generated.

Nociceptors detect tissue damage, triggering peripheral sensitization and primary hyperalgesia. Neuroplasticity explains nervous system adaptation and is key for rehabilitation, influencing pain perception and chronicization.

Keywords:
EndocannabinoidsHyperalgesic primingPKCTRP channelsneurotrophic factors

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Area of Science:

  • Neuroscience
  • Pain Research
  • Molecular Biology

Background:

  • Nociceptors detect tissue damage and initiate pain signals.
  • Peripheral sensitization amplifies pain responses to acute injury.
  • Neuroplasticity underlies nervous system adaptation to stimuli and is crucial for rehabilitation.

Purpose of the Study:

  • To review studies on nociceptor receptors and ion channels in pain perception.
  • To explore the role of neuroplasticity in adapting to harmful stimuli.
  • To examine mediators involved in central sensitization and pain chronicization.

Main Methods:

  • Literature review of studies on nociceptors, ion channels, and mediators.
  • Analysis of research addressing neuroplasticity in pain pathways.
  • Examination of mechanisms leading to central sensitization.

Main Results:

  • Changes in nociceptor receptors and ion channels are linked to neuroplasticity.
  • Inflammatory mediators contribute to peripheral sensitization and primary hyperalgesia.
  • Prolonged nociception can lead to central sensitization and pain memory.

Conclusions:

  • Nociceptor function is modulated by neuroplastic changes in receptors and ion channels.
  • Understanding these mechanisms is vital for developing effective pain management and rehabilitation strategies.
  • Neuroplasticity plays a significant role in both acute pain processing and the chronicization of pain perception.