Group A nerve fiber
Group A nerve fibers are one of the three classes of nerve fiber as generally classified by Erlanger and Gasser. The other two classes are the group B nerve fibers, and the group C nerve fibers. Group A are heavily myelinated, group B are moderately myelinated, and group C are unmyelinated.[1]
The other classification is a sensory grouping that uses the terms type Ia and type Ib, type II, type III, and type IV, sensory fibers.[1]
Types
There are four subdivisions of group A nerve fibers: alpha (α) Aα; beta (β) Aβ; , gamma (γ) Aγ, and delta (δ) Aδ. These subdivisions have different amounts of myelination and axon thickness and therefore transmit signals at different speeds. Larger diameter axons and more myelin insulation lead to faster signal propagation.
Group A nerves are found in both motor and sensory pathways.
| Type | Erlanger-Gasser Classification | Diameter | Myelin | Conduction velocity | Associated muscle fibers |
|---|---|---|---|---|---|
| α | Aα | 13–20 μm | Yes | 80–120 m/s | Extrafusal muscle fibers |
| γ | Aγ | 5–8 μm | Yes | 4–24 m/s [2][3] | Intrafusal muscle fibers |
Different sensory receptors are innervated by different types of nerve fibers. Proprioceptors are innervated by type Ia, Ib and II sensory fibers, mechanoreceptors by type II and III sensory fibers, and nociceptors and thermoreceptors by type III and IV sensory fibers.
| Type | Erlanger-Gasser Classification | Diameter | Myelin | Conduction velocity | Associated sensory receptors |
|---|---|---|---|---|---|
| Ia | Aα | 13–20 μm | Yes | 80–120 m/s[4] | Responsible for proprioception |
| Ib | Aα | 13–20 μm | Yes | 80–120 m/s | Golgi tendon organ |
| II | Aβ | 6–12 μm | Yes | 33–75 m/s | Secondary receptors of muscle spindle All cutaneous mechanoreceptors Some Nociceptors[5] |
| III | Aδ | 1–5 μm | Thin | 3–30 m/s | Free nerve endings of touch and pressure Nociceptors of neospinothalamic tract Cold thermoreceptors |
| IV | C | 0.2–1.5 μm | No | 0.5–2.0 m/s | Nociceptors of paleospinothalamic tract Warmth receptors |
Type Aα fibers include the type Ia and type Ib sensory fibers of the alternative classification system, and are the fibers from muscle spindle endings and the Golgi tendon, respectively.[1]
Type Aβ fibres, and type Aγ, are the type II afferent fibers from stretch receptors.[1] Type Aβ fibres from the skin are mostly dedicated to touch. However a small fraction of these fast fibres, termed "ultrafast nociceptors", also transmit pain.[5]
Type Aδ fibers are the afferent fibers of nociceptors. Aδ fibers carry information from peripheral mechanoreceptors and thermoreceptors to the dorsal horn of the spinal cord. This pathway describes the first-order neuron. Aδ fibers serve to receive and transmit information primarily relating to acute pain (sharp, immediate, and relatively short-lasting). This type of pain can result from several classifications of stimulants: temperature-induced, mechanical, and chemical. This can be part of a withdrawal reflex—initiated by the Aδ fibers in the reflex arc of activating withdrawal responses.[6][7] These are the type III group. Aδ fibers carry cold, pressure, and acute pain signals; because they are thin (2–5 μm in diameter) and myelinated, they send impulses faster than unmyelinated C fibers, but more slowly than other, more thickly myelinated group A nerve fibers. Their conduction velocities are moderate.[8]
Their cell bodies are located in the dorsal root ganglia and axons are sent to the periphery to innervate target organs and are also sent through the dorsal roots to the spinal cord. Within the spinal cord the axons reach the posterior grey column and terminate in Rexed laminae I to V.[9]
References
- 1 2 3 4 Hall, John (2011). Guyton and Hall textbook of medical physiology (12th ed.). Philadelphia, Pa.: Saunders/Elsevier. pp. 563–564. ISBN 978-1-4160-4574-8.
- ↑ Andrew, BL; Part, NJ (1972). "Properties of fast and slow motor units in hind limb and tail muscles of the rat". Quarterly Journal of Experimental Physiology and Cognate Medical Sciences. 57 (2): 213–225. doi:10.1113/expphysiol.1972.sp002151. PMID 4482075.
- ↑ Russell NJ (1980). "Axonal conduction velocity changes following muscle tenotomy or deafferentation during development in the rat". J Physiol. 298: 347–360. doi:10.1113/jphysiol.1980.sp013085. PMC 1279120. PMID 7359413.
- ↑ Siegel, Allan; Sapru, Hreday (2005). Essential Neuroscience. p. 257. ISBN 978-0781750776.
- 1 2 Nagi, Saad S.; Marshall, Andrew G.; Makdani, Adarsh; Jarocka, Ewa; Liljencrantz, Jaquette; Ridderström, Mikael; Shaikh, Sumaiya; O’Neill, Francis; Saade, Dimah; Donkervoort, Sandra; Foley, A. Reghan; Minde, Jan; Trulsson, Mats; Cole, Jonathan; Bönnemann, Carsten G.; Chesler, Alexander T.; Bushnell, M. Catherine; McGlone, Francis; Olausson, Håkan (2019). "An ultrafast system for signaling mechanical pain in human skin". Science Advances. 5 (7): eaaw1297. Bibcode:2019SciA....5.1297N. doi:10.1126/sciadv.aaw1297. ISSN 2375-2548. PMC 6609212. PMID 31281886.
- ↑ Skljarevski, V.; Ramadan, N. M. (2002). "The nociceptive flexion reflex in humans – review article". Pain. 96 (1): 3–8. doi:10.1016/s0304-3959(02)00018-0. PMID 11932055. S2CID 23881420.
- ↑ 1962-, Striedter, Georg F. (2016). Neurobiology : a functional approach (Instructor's ed.). New York. ISBN 9780195396157. OCLC 919041751.
{{cite book}}: CS1 maint: numeric names: authors list (link) - ↑ Neuroscience. Purves, Dale. (5th ed.). Sunderland, Mass.: Sinauer Associates. 2012. ISBN 9780878936953. OCLC 754389847.
{{cite book}}: CS1 maint: others (link) - ↑ Basbaum, Allan I.; Bautista, Diana M.; Scherrer, Grégory; Julius, David (October 2009). "Cellular and Molecular Mechanisms of Pain". Cell. 139 (2): 267–284. doi:10.1016/j.cell.2009.09.028. PMC 2852643. PMID 19837031.