Group A nerve fiber

(Redirected fromA delta fiber)

Group A nerve fibersare one of the three classes ofnerve fiberasgenerally classifiedbyErlangerandGasser.The other two classes are thegroup B nerve fibers,and thegroup C nerve fibers.Group A are heavilymyelinated,group B are moderatelymyelinated,and group C are unmyelinated.[1][2]

The other classification is asensorygrouping that uses the termstype Ia and type Ib,type II,type III,andtype IV,sensory fibers.[1]

Types

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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 andthereforetransmit signals atdifferent speeds.Larger diameter axons and more myelin insulation lead to faster signal propagation.

Group A nerves are found in both motor and sensory pathways.[2]

Motor fiber types
Type Erlanger-Gasser
Classification
Diameter Myelin Conduction velocity Associatedmuscle fibers
α 13–20μm Yes 80–120 m/s Extrafusal muscle fibers
γ 5–8μm Yes 4–24 m/s[3][4] Intrafusal muscle fibers

Differentsensory receptorsare innervated by different types of nerve fibers.Proprioceptorsare innervated by type Ia, Ib and II sensory fibers,mechanoreceptorsby type II and III sensory fibers, andnociceptorsandthermoreceptorsby type III and IV sensory fibers.

Sensory fiber types
Type Erlanger-Gasser
Classification
Diameter Myelin Conduction velocity Associatedsensory receptors
Ia 13–20μm Yes 80–120 m/s[5] Muscle spindle fibres
Ib 13–20μm Yes 80–120 m/s Golgi tendon organ
II 6–12μm Yes 33–75 m/s Allcutaneous mechanoreceptorsincludingpacinian corpuscles
III 1–5μm Thin 3–30 m/s Free nerve endingsof touch and pressure
Nociceptorsofneospinothalamic tract
Coldthermoreceptors
IV C 0.2–1.5μm No 0.5–2.0 m/s Nociceptorsofpaleospinothalamic tract
Warmth receptors

Type Aα fibers include thetype Iaandtype Ibsensory fibers of the alternative classification system, and are the fibers frommuscle spindleendings and theGolgi tendon,respectively.[1]

Type Aβ fibres, and type Aγ, are thetype IIafferent fibersfromstretch 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.[6]

Type Aδ fibers are theafferent fibersofnociceptors.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 toacute 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 awithdrawal reflex—initiated by the Aδ fibers in thereflex arcof activating withdrawal responses.[7][8]These are thetype IIIgroup. Aδ fibers carry cold, pressure, and acute pain signals; because they are thin (2–5 μm in diameter) andmyelinated,they send impulses faster than unmyelinatedC fibers,but more slowly than other, more thickly myelinated group A nerve fibers. Theirconduction velocitiesare moderate.[9]

Theircell bodiesare located in thedorsal root gangliaand 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 theposterior grey columnand terminate in Rexed laminae I to V.[10]

References

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  1. ^abcdHall, John (2011).Guyton and Hall textbook of medical physiology(12th ed.). Philadelphia, Pa.: Saunders/Elsevier. pp. 563–564.ISBN978-1-4160-4574-8.
  2. ^ab"Classification of Nerve Fibers".pharmacy180.com.RetrievedSeptember 6,2023.
  3. ^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.PMID4482075.
  4. ^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.PMC1279120.PMID7359413.
  5. ^Siegel, Allan; Sapru, Hreday (2005).Essential Neuroscience.Lippincott Williams & Wilkins. p.257.ISBN978-0781750776.
  6. ^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.ISSN2375-2548.PMC6609212.PMID31281886.
  7. ^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.PMID11932055.S2CID23881420.
  8. ^Striedter, Georg F. (2016).Neurobiology: a functional approach(Instructor's ed.). New York.ISBN9780195396157.OCLC919041751.{{cite book}}:CS1 maint: location missing publisher (link)
  9. ^Neuroscience.Purves, Dale. (5th ed.). Sunderland, Mass.: Sinauer Associates. 2012.ISBN9780878936953.OCLC754389847.{{cite book}}:CS1 maint: others (link)
  10. ^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.PMC2852643.PMID19837031.