Type II sensory fiber

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Type II sensory fiber (group Aβ) is a type of sensory fiber, the second of the two main groups of stretch receptors. They are non-adapting, meaning that even when there is no change in muscle length, they keep responding to stimuli. In the body, Type II fibers are the second most highly myelinated fibers. Type II sensory neurons are pseudounipolar and their reside in ganglia either in the dorsal horn or the brainstem.[1]

The muscle's instantaneous length, or position, is directly proportional to their firing rate. This information would indicate the position of one's leg once it has stopped moving. They do not respond to rate of length changes as do the Ia fibers.[2]

Type II fibers connect to nuclear chain fibers and static nuclear bag fibers in muscle spindles, but not to dynamic nuclear bag fibers. The typical innervation to muscle spindles consists of one type I fiber and 2 type II fibers.[3] These connections, referred to as "flower spray endings" due to their appearance, embed into the poles (ends) of the fibre. It is thought that the relative position of the equatorial regions of the spray when stretched determines the action potential output.

Type II fibers assist in the transmission of somatosensory information as well as nociceptive information. In normal physiological conditions they transmit tactile touch, the responses of different type II fibers to these stimuli can be subdivided based on their adaptation properties, traditionally into rapidly adapting(RA) or slowly adapting(SA) neurons.[4] Type II RA neurone endings can take the form of Meissner's corpuscles, Pacinian corpuscles, or Lanceolate Endings, whereas type II SA neurone endings are Merkel cell-neurite complexes or Ruffini endings. Under pathological conditions they may become hyper-excitable leading to stimuli that would usually elicit sensations of tactile touch causing pain.[5] These changes are in part induced by PGE2 which is produced by COX1, and type II fibers with free nerve endings are likely to be the subdivision of fibers that carry out this function.[5][6]

References[edit]

  1. ^ de Moraes ER, Kushmerick C, Naves LA (October 2017). "Morphological and functional diversity of first-order somatosensory neurons". Biophysical Reviews. 9 (5): 847–856. doi:10.1007/s12551-017-0321-3. PMID 28889335. 
  2. ^ Niessen MH, Veeger DH, Koppe PA, Konijnenbelt MH, van Dieën J, Janssen TW (February 2008). "Proprioception of the shoulder after stroke". Archives of Physical Medicine and Rehabilitation. 89 (2): 333–8. doi:10.1016/j.apmr.2007.08.157. PMID 18226659. 
  3. ^ Poliak S, Norovich AL, Yamagata M, Sanes JR, Jessell TM (January 2016). "Muscle-type Identity of Proprioceptors Specified by Spatially Restricted Signals from Limb Mesenchyme". Cell. 164 (3): 512–25. doi:10.1016/j.cell.2015.12.049. PMC 4733250Freely accessible. PMID 26824659. 
  4. ^ Olson W, Dong P, Fleming M, Luo W (2016-05-01). "The specification and wiring of mammalian cutaneous low-threshold mechanoreceptors". Wiley Interdisciplinary Reviews. Developmental Biology. 5 (3): 389–404. doi:10.1002/wdev.229. PMID 26992078. 
  5. ^ a b Sun W, Yang F, Wang Y, Fu H, Yang Y, Li CL, Wang XL, Lin Q, Chen J (February 2017). "Contribution of large-sized primary sensory neuronal sensitization to mechanical allodynia by upregulation of hyperpolarization-activated cyclic nucleotide gated channels via cyclooxygenase 1 cascade". Neuropharmacology. 113 (Pt A): 217–230. doi:10.1016/j.neuropharm.2016.10.012. PMID 27743933. 
  6. ^ Arcourt A, Gorham L, Dhandapani R, Prato V, Taberner FJ, Wende H, Gangadharan V, Birchmeier C, Heppenstall PA, Lechner SG (January 2017). "Touch Receptor-Derived Sensory Information Alleviates Acute Pain Signaling and Fine-Tunes Nociceptive Reflex Coordination". Neuron. 93 (1): 179–193. doi:10.1016/j.neuron.2016.11.027. PMID 27989460.