Group C nerve fiber

Source: Wikipedia, the free encyclopedia.

Group C nerve fiber
nerve fiber
Anatomical terms of neuroanatomy]

Group C nerve fibers are one of three classes of

postganglionic fibers
in the
dorsal roots
(IV fiber). These fibers carry sensory information.

Damage or injury to nerve fibers causes neuropathic pain. Capsaicin activates C fibre vanilloid receptors, giving chili peppers a hot sensation.

Structure and anatomy

Location

C fibers are one class of

nerves of the somatic sensory system.[1] They are afferent fibers, conveying input signals from the periphery to the central nervous system.[2]

Structure

C fibers are

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 m/s.[1] C fibers are on average 0.2-1.5 μm
in diameter.

Remak bundles

C fiber axons are grouped together into what is known as Remak bundles.[3] These occur when a non-myelinating Schwann cell bundles the axons close together by surrounding them.[4] The Schwann cell keeps them from touching each other by squeezing its cytoplasm between the axons.[4] The condition of Remak bundles varies with age.[4] The number of C fiber axons in each Remak bundle varies with location.[3] For example, in a rat model, large bundles of greater than 20 axons are found exiting the L5 dorsal root ganglion, while smaller bundles of average 3 axons are found in distal nerve segments.[3] Multiple neurons contribute axons to the Remak bundle with an average ratio of about 2 axons contributed per bundle.[3] The cross sectional area of a Remak bundle is proportional to the number of axons found inside it.[3] Remak bundles in the distal peripheral nerve are clustered with other Remak bundles.[3] The Remak Schwann cells have been shown to be electrochemically responsive to action potentials of the axons contained within them.[3]

In experiments where nerve injury is caused but nearby C fibers remain intact, increased spontaneous activity in the C fibers is observed.

neuropathic pain.[3] Remak bundles are thought to release certain trophic factors that promote the regeneration of the damaged axons.[3]

Pathway

C fibers synapse to second-order projection neurons in the spinal cord at the upper laminae of the

brain stem and thalamus in the ventrolateral, or anterolateral, quadrant of the contralateral half of the spinal cord, forming the spinothalamic tract.[1] The spinothalamic tract is the main pathway associated with pain and temperature perception, which immediately crosses the spinal cord laterally.[1]
This crossover feature is clinically important because it allows for identification of the location of injury.

Function

Because of their higher conduction velocity owing to strong myelination and different activation conditions, Aδ fibers are broadly responsible for the sensation of a quick shallow pain that is specific on one area, termed as first pain.[1] They respond to a weaker intensity of stimulus.[1] C fibers respond to stimuli which have stronger intensities and are the ones to account for the slow, lasting and spread out second pain.[1] These fibers are virtually unmyelinated and their conduction velocity is, as a result, much slower which is why they presumably conduct a slower sensation of pain.[7]

C fibers are considered polymodal because they can react to various stimuli. They react to stimuli that are thermal, or mechanical, or chemical in nature.

hypoxia, hypoglycemia, hypo-osmolarity, the presence of muscle metabolic products, and even light or sensitive touch.[8]
C fiber receptors include:

This variation of input signals calls for a variety of cells of the cortex in lamina 1 to have different modality-selectiveness and morphologies.[8] These varying neurons are responsible for the different feelings we perceive in our body and can be classified by their responses to ranges of stimuli.[8] The brain uses the integration of these signals to maintain homeostasis in the body whether it is temperature related or pain related.[8]

Vanilloid receptor

The

transient receptor potential (TRP) receptors.[1] If damage to these heat transducer receptors occurs, the result can be chronic neuropathic pain caused by lowering the heat pain threshold for their phosphorylation.[9][12]

Role in neuropathic pain

Activation of nociceptors is not necessary to cause the sensation of pain.[12] 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.[12] Neuropathic pain syndromes are caused by lesions or diseases of the parts of the nervous system that normally signal pain.[13] There are four main classes:

After a nerve lesion of either C fibers or Aδ fibers, they become abnormally sensitive and cause

hyperactivity.[14]

Central sensitization

After nerve damage or repeated stimulation, WDR (wide dynamic range) neurons experience a general increase in excitability.[5] This hyper-excitability can be caused by an increased neuronal response to a noxious stimulus (hyperalgesia), a larger neuronal receptive field, or spread of the hyper-excitability to other segments.[5] This condition is maintained by C fibers.[5]

C fibers cause central sensitization of the dorsal horn in the spinal cord in response to their hyperactivity.

Nitric Oxide Synthase. Nitric Oxide is thought to migrate back to the presynaptic membrane to enhance the expression of the voltage-gated N-calcium channels resulting in a pain wind-up phenomenon. This abnormal central sensitization cycle results in increased pain (hyperalgesia) and pain responses from previously non-noxious stimuli (allodynia).[5]

Central sensitization of the dorsal horn neurons that is evoked from C fiber activity is responsible for temporal summation of "second pain" (TSSP).[15] This event is called ‘windup’ and relies on a frequency greater or equal to 0.33Hz of the stimulus.[15] Windup is associated with chronic pain and central sensitization.[15] This minimum frequency was determined experimentally by comparing healthy patient fMRI's when subjected to varying frequencies of heat pulses.[15] 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).[15] 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.[15]

Treatment

Currently, the availability of drugs proven to treat neuropathic pain is limited and varies widely from patient to patient.[12] Many developed drugs have either been discovered by accident or by observation.[12] Some past treatments include opiates like poppy extract, non-steroidal anti-inflammatory drugs like salicylic acid, and local anesthetics like cocaine.[12] Other recent treatments consist of antidepressants and anticonvulsants, although no substantial research on the actual mechanism of these treatments has been performed.[12] However, patients respond to these treatments differently, possibly because of gender differences or genetic backgrounds.[12] Therefore, researchers have come to realize that no one drug or one class of drugs will reduce all pain.[12] 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.[12]

Microneurography

postganglionic sympathetic C fibers of the muscles and skin yield insights into the neural control of autonomic effector organs like blood vessels and sweat glands.[16] Readings of afferent discharges from C nociceptors identified by marking method have also proved helpful in revealing the mechanisms underlying sensations such as itch.[16]

Unfortunately, interpretation of the microneurographic readings can be difficult because axonal membrane potential can not be determined from this method.[17] 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.[17] Moalem-Taylor et al. experimentally used chemical modulators with known effects on membrane potential to study the post-spike super-excitability of C fibers.[17] The researchers found three resulting events.[17] Chemical modulators can produce a combination of loss of super-excitability along with increased axonal excitability, indicating membrane depolarization.[17] Secondly, membrane hyperpolarization can result from a blockade of axonal hyperpolarization-activated current.[17] 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.[17]

See also

References

  1. ^
    ISBN 978-0-87893-725-7
    .
  2. S2CID 17829407
    .
  3. ^
    PMID 15055448
    .
  4. ^ a b c Fagan, Tom (2003). "Glial Cells Critical for Peripheral Nervous System Health". News from Harvard Medical, Dental and Public Health Schools.
  5. ^
    S2CID 12925061
    .
  6. ^
    PMID 114611
    .
  7. PMID 30042373
    .
  8. ^
    S2CID 16369323
    .
  9. ^
    S2CID 4311541
    .
  10. ^
    ISBN 978-0-87893-695-3
    .
  11. ^
    S2CID 4337894
    .
  12. ^
    S2CID 15781811
    .
  13. PMID 10870735
    .
  14. ^
    S2CID 24745129
    .
  15. ^
    PMID 17156923
    .
  16. ^
    S2CID 22258173
    .
  17. ^
    S2CID 36126632
    .
Retrieved from "https://en.wikipedia.org/w/index.php?title=Group_C_nerve_fiber&oldid=1191209104"