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Primary afferent nociceptors

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Primary afferent nociceptors

Claudia Cheng

Updated in August 2006

Primary afferent nociceptors are specialized free nerve endings of primary afferent nerves (A-delta and C fibres). They are generally the first structures to be involved in the nociceptive process and are located in various body tissues including skin, muscle, connective tissue, blood vessels and thoracic and abdominal viscera. The skin is supplied by A-delta and C-nociceptors/fibres. Muscles, joints, fasciae and other deep somatic structures are supplied mainly by C- but also some A-delta nociceptors/fibres.

 

A-delta nociceptors are activated by mechanical and thermal stimuli. A-delta fibres are the smallest of the myelinated nerves. They are 2-5 um in diameter and are fast with a conduction velocity of 6-30 m/s. Activation of A-delta fibres results in short-lasting, pricking-type pain

 

C nociceptors are polymodal (mechanical, thermal, chemical). C-fibres are unmyelinated, less than 2 um in diameter and have a slow conduction velocity of 0.5-2 um/s. Activation of C fibres results in dull, poorly localized, burning type pain

 

Stimulation of these nociceptors occurs when the pain threshold is reached. This then results in propagation of impulses along the afferent fibres toward the dorsal horn of the spinal cord (periphery) or to the medulla (cranial). Stimulation of the primary afferent nociceptors which result in pain can be from

1)      physical stimuli – mechanical injury, noxious heat, radiation

2)      byproducts of tissue damage resulting in release of cellular contents and mediators from the nociceptive afferents. Chemicals released from damaged cells include bradykinin, potassium, serotonin, histamine, cytokines, nitric oxide, hydrogen ions, prostaglandins, leukotrienes, slow reacting substance of anaphylaxis. Mediators released from the afferent nociceptors include substance P, calcitonin-gene-related peptide, neurokinins.

 

After a brief period of noxious stimulation, peripheral sensitization occurs. This is a normal physiological response to pain. The mechanism involves release of intracellular contents from damaged cells and inflammatory cells, collectively known as the “inflammatory soup”. In the presence of this “soup”, the sensitivity of the primary afferent nociceptors is increased, there is lowered threshold to stimulation and there is prolonged and enhanced response to the stimulation. Clinically, this is manifested as primary hyperalgesia

 Ó Claudia Cheng August 2006

 


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