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Group C nerve fibers

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Group C nerve fibers
Medulla spinalis - Substantia grisea - English
Latin '
Gray's subject #
MeSH [1]

Structure and AnatomyEdit


C fibers are found in the peripheral nerves of the somatic sensory system.[1] They convey the sense of the physiological condition of the body from the periphery to the central nervous system.[2]


C fibres are unmyelinated unlike most other fibers in the nervous system. [1] This lack of myelination is the cause of their slow conduction velocity, which is on the order of no more than 2 Template:Val/unitswithlink.[1] C fibers are on average 0.2-1.5 μm in diameter.[1] The other main classification of nociceptors is Aδ fibers.[1] These fibers have axons that are larger (1-5 μm), in diameter, are myelinated, and have a higher conduction velocity, which is on the order of about 20 m/s.[1]

Remak bundlesEdit






Because of their higher conduction velocity, Aδ fibers are responsible for the sensation of a sharp first pain.[1] They respond to a weaker intensity of stimulus.[1] C fibers, however, respond to a stronger intensity of stimulus and are responsible for the slow, dull, longer-lasting, second pain.[1]

C fibers are considered polymodal because they can respond to thermal, mechanical, and chemical stimuli.[1] C fibers respond to all kinds of physiological changes in the body.[7] For example, they can respond to hypoxia, hypoglycemia, hypo-osmolarity, the presence of muscle metabolic products, and even light or sensitive touch.[7] C fiber receptors include:

  • C fiber nociceptors
    • responsible for the second, burning pain
  • C fiber warming specific receptors
    • responsible for warmth
  • ultra-slow histamine-selective C fibers
    • responsible for itch
  • tactile C fibers
    • sensual touch
  • C mechano- and metabo- receptors in muscles or joints
    • responsible for muscle exercise, burn and cramp[7]


Vanilloid ReceptorEdit


Role in Neuropathic PainEdit

Activation of nociceptors is not necessary to cause the sensation of pain.[9] Damage or injury to nerve fibers that normally respond to innocuous stimuli like light touch may lower their activation threshold needed to respond; this change causes the organism to feel intense pain from the lightest of touch.[9] Neuropathic pain syndromes are caused by lesions or diseases of the parts of the nervous system that normally signal pain.[10] There are four main classes:


Central SensitizationEdit


Central sensitization of the dorsal horn neurons that is evoked from C fiber activity is responsible for temporal summation of “second pain” (TSSP).[12] This event is called ‘windup’ and relies on a frequency greater or equal to 0.33Hz of the stimulus.[12] Windup is associated with chronic pain and central sensitization.[12] This minimum frequency was determined experimentally by comparing healthy patient fMRI’s when subjected to varying frequencies of heat pulses.[12] The fMRI maps show common areas activated by the TSSP responses which include contralateral thalamus (THAL), S1, bilateral S2, anterior and posterior insula (INS), mid-anterior cingulate cortex (ACC), and supplemental motor areas (SMA).[12] TSSP events are also associated with other regions of the brain that process functions such as somatosensory processing, pain perception and modulation, cognition, pre-motor activity in the cortex.[12]


Currently, the availability of drugs proven to treat neuropathic pain is limited and varies widely from patient to patient.[9] Many developed drugs have either been discovered by accident or by observation.[9] Some past treatments include opiates like poppy extract, non-steroidal anti-inflammatory drugs like salicylic acid, and cocaine.[9] Other recent treatments consist of antidepressants and anticonvulsants, although no substantial research on the actual mechanism of these treatments has been performed.[9] However, patients respond differently to these treatments possibly because of gender differences or genetic backgrounds.[9] Therefore, researchers have come to realize that no one drug or one class of drugs will reduce all pain.[9] Research is now focusing on the underlying mechanisms involved in pain perception and how it can go wrong in order to develop an appropriate drug for patients afflicted with neuropathic pain.[9]


Microneurography is a technique using metal electrodes to observe neural traffic of both myelinated and unmyelinated axons in efferent and afferent neurons of the skin and muscle.[13] This technique is particularly important in research involving C fibers.[13] Single action potentials from unmyelinated axons can be observed.[13] Recordings from efferent postganglionic sympathetic C fibers of the muscles and skin yield important insights into the neural control autonomic effector organs like blood vessels and sweat glands.[13] Readings of afferent discharges from C nociceptors identified by marking method have also proved as important tools to revealing the mechanisms underlying sensations such as itch.[13]

Unfortunately, interpretation of the microneurographic readings can be difficult because axonal membrane potential can not be determined from this method.[14] A supplemental method used to better understand these readings involves examining recordings of post-spike excitability and shifts in latency; these features are associated with changes in membrane potential of unmyelinated axons like C fibers.[14] Moalem-Taylor et al. experimentally used chemical modulators with known effects on membrane potential to study the post-spike super-excitability of C fibers.[14] The researchers found three resulting events.[14] Chemical medulators can produce a combination of loss of super-excitability along with increased axonal excitability, indicating membrane depolarization.[14] Secondly, membrane hyperpolarization can result from a blockade of axonal hyperpolarization-activated current.[14] Lastly, a non-specific increase in surface charge and a change in the voltage-dependent activation of sodium channels results from the application of calcium.[14]

See alsoEdit


  1. 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 1.17 1.18 Purves, Dale; (2004). Neuroscience, Massachusetts: Sinauer Associates, Inc..
  2. (Aug 2002). How do you feel? Interoception: the sense of the physiological condition of the body. Nature Reviews Neuroscience 3 (8): 655—66.
  3. 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 3.11 3.12 Murinson, BB, JW Griffin (2004). C-fiber structure varies with location in peripheral nerve. Journal of Neuropathology and Experimental Neurology 63: 246–254.
  4. 4.0 4.1 4.2 Fagan, Tom (2003). Glial Cells Critical for Peripheral Nervous System Health. News from Harvard Medical, Dental and Public Health Schools.
  5. 5.00 5.01 5.02 5.03 5.04 5.05 5.06 5.07 5.08 5.09 5.10 5.11 5.12 5.13 Baron, Ralph (2006). Mechanisms of Disease: neuropathic pain—a clinical perspective. Nature Clinical Practice Neurology 2.
  6. 6.0 6.1 Chung, J.M., et. al (1979). Excitation of primate spinothalamic neurons by cutaneous C-fiber volleys. .” Journal of Neurophysiology 42: 1354–1369.
  7. 7.0 7.1 7.2 7.3 7.4 7.5 Craig, AD (2003). Interoception: the sense of the physiological condition of the body. Current Opinion in Neurobiology 13: 500–505.
  8. 8.0 8.1 Davis, JB, et. al (2000). Vanilloid receptor-1 is essential for inflammatory thermal hyperalgesia. Nature 405: 183–7.
  9. 9.0 9.1 9.2 9.3 9.4 9.5 9.6 9.7 9.8 9.9 Scholz, Joachim, Clifford Woolf (2002). Can we conquer pain?. Nature Neuroscience 5: 1062–1067.
  10. Baron, Ralph (2000). Peripheral neuropathic pain: from mechanisms to symptoms. Clinical Journal of Pain 16: S12–20.
  11. 11.0 11.1 Lai, J (2003). The role of voltage-gated sodium channels in neuropathic pain. Current Opinion Neurobiology 13: 291–297.
  12. 12.0 12.1 12.2 12.3 12.4 12.5 Staud, Roland, et. al (2007). Brain activity related to temporal summation of C-fiber evoked pain. Pain 129: 130–142.
  13. 13.0 13.1 13.2 13.3 13.4 Mano, Tadaaki, et. al (2006). Microneurography as a tool in clinical neurophysiology to investigate peripheral neural traffic in humans. Clinical Neurophysiology 117: 2357–2384.
  14. 14.0 14.1 14.2 14.3 14.4 14.5 14.6 Moalem-Taylor, Gila, et. al (2007). Post-spike excitability indicates changes in membrane potential of isolated c-fibers. Muscle and Nerve 36: 172–182.


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