Group C nerve fiber
Group C nerve fiber | |
---|---|
nerve fiber | |
Anatomical terms of neuroanatomy] |
Group C nerve fibers are one of three classes of
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
Structure
C fibers are
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.
Pathway
C fibers synapse to second-order projection neurons in the spinal cord at the upper laminae of the
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.
- 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
- includes CT fibres, also known as C low-threshold mechanoreceptors (CLTM), which are unmyelinated afferents found in human hairy skin, and have a low mechanical threshold < 5 milliNewtons. They have moderate adaptation and may exhibit fatigue on repetitive stimulation and "afterdischarges" for several seconds after a stimulus.[9]
- C mechano- and metabo- receptors in muscles or joints
- responsible for muscle exercise, burn and cramp[8]
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
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:
- peripheral focal and multifocal nerve lesions
- traumatic, ischemic or inflammatory
- peripheral generalized polyneuropathies
- toxic, metabolic, hereditary or inflammatory
- CNS lesions
- stroke, multiple sclerosis, spinal cord injury
- complex neuropathic disorders
After a nerve lesion of either C fibers or Aδ fibers, they become abnormally sensitive and cause
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.
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
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]
Philosophical Relevance
C fibers have repeatedly by calling it scientifically unjustified.
See also
- A nerve fibers
- B nerve fibers
- Free nerve ending
- Nociceptor
- Pain and nociception
- Sensory neuron
- Thermoreceptor
References
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- ^ PMID 15055448.
- ^ a b c Fagan, Tom (2003). "Glial Cells Critical for Peripheral Nervous System Health". News from Harvard Medical, Dental and Public Health Schools.
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- ^ PMID 114611.
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- ^ S2CID 16369323.
- ^ S2CID 4311541.
- ^ ISBN 978-0-87893-695-3.
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- ^ PMID 17156923.
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- ^ "David Lewis | Internet Encyclopedia of Philosophy". Retrieved April 23, 2024.
- JSTOR 187355.
- ^ "Identity Theory | Internet Encyclopedia of Philosophy". Retrieved April 23, 2024.
- ^ Aranyosi, István (April 23, 2024). "The Peripheral Mind: Philosophy of Mind and the Peripheral Nervous System | Return of the C Fibers; or, Philosophers' Lack of Nerve". academic.oup.com. OUP. pp. 34–57. Retrieved April 23, 2024.