Neurogenic inflammation

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Neurogenic Inflammation

Neurogenic inflammation (/nʊərəʊˈdʒɛnɪk ɪnfləˈmeɪʃən/) is a type of inflammation that results from the release of various substances from sensory nerve endings. These substances, which include neuropeptides such as substance P and calcitonin gene-related peptide (CGRP), can cause blood vessels to dilate and become more permeable, leading to the characteristic signs of inflammation: redness, heat, swelling, and pain.

Etymology

The term "neurogenic" is derived from the Greek words "neuron" (nerve) and "genesis" (origin), indicating that the inflammation originates from the nervous system. The term "inflammation" comes from the Latin "inflammatio", meaning "a setting on fire", which refers to the heat and redness associated with this condition.

Mechanism

Neurogenic inflammation is initiated when nociceptors, or pain-sensing nerve endings, are activated by harmful stimuli such as injury, infection, or exposure to certain chemicals. This activation triggers the release of neuropeptides, which then act on nearby blood vessels and immune cells to produce the signs of inflammation.

Related Terms

  • Nociceptor: A type of sensory nerve ending that responds to potentially damaging stimuli by sending signals to the spinal cord and brain.
  • Neuropeptide: A type of molecule used by neurons to communicate with each other.
  • Substance P: A neuropeptide involved in the transmission of pain signals.
  • Calcitonin gene-related peptide (CGRP): A neuropeptide that plays a key role in the dilation of blood vessels and the transmission of pain signals.

External links

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