Table 3.Download Silmarillion Torrent at TorrentFunk. Neurotrophins are thought to play an important part in this. This is important for the development of mechanical allodynia which is mediated by A-beta fibres ( Coderre et al 2003). After inflammation or injury A-beta fibres can produce and release SP which they do not contain under normal circumstances. Primary afferent neurons can switch their phenotype as the result of changes in gene expression leading to an up-regulation of various transmitters, receptors, ion channels and growth factors (Table 3.3). Sensory neurons remain responsive to neurotrophic factors into adulthood and they have effects on the pain experience. A-delta fibres express the high-affinity receptor for neurotrophin 3 and tyrosine kinase C. Tyrosine kinase activity continues in the remaining half of C-fibres. These neurons become the non-peptidergic C-fibres and express surface glucoconjugates that bind the lectin IB4 ( Molliver et al 1997). Most of these fibres switch to expressing Ret, the transmembrane signalling component of the receptor for glial cell-derived neurotrophic factor (GDNF) as well as other neurotrophic factors (McMahon et al 2006). During perinatal and postnatal development approximately half the nociceptive population switch off the genes necessary for (TrkA) expression. Nociceptive neurons develop from neural crest stem cells that migrate from the dorsal part of the neural tube and are formed late in neurogenesis under the neurotrophic influence of nerve growth factor (NGF) interacting with the tyrosine kinase A (trkA) receptor in the periphery. This plasticity allows mediation of homeostatic functions under physiological conditions and sensitization following injury or inflammation. Nociceptors are dynamic and shift their properties according to their environment ( Schmidt et al 1994). Peptidergic and non-peptidergic fibres have different processes of signal transduction and demonstrate different sensitivities to the same stimulus (McMahon et al 2006). Non-peptidergic neurons project to areas within lamina II and contain only neurotransmitters. Peptidergic C-fibres project mainly to lamina I and lamina II outer layers of the dorsal horn. Peptidergic nociceptive neurons also contain excitatory neurotransmitters (glutamate). The majority of peptidergic neurons co-localize substance P (SP) and calcitonin gene-related peptide (CGRP) whilst others contain vasoactive intestinal peptide (VIP) and somatostatin (SS) (Woolf & Ma 2007). Nociceptive neurons are further divided into two major subgroups: those expressing peptides (peptidergic) and those that do not (non-peptidergic). Nociceptive neurons are also found in viscera, but there are relatively fewer A-delta fibres. The concentration of nociceptive neurons within a tissue is positively correlated to that tissue’s sensitivity to pain. Nociceptive neurons are found in somatic tissues such as skin, joints, muscle, fascia, tendons, cornea and tooth pulp ( Cimino 1992). These have very high thresholds for mechanical stimulation and do not fire under normal circumstances ( Meyer et al 2006). Both C and A-delta fibres may be associated with ‘silent nociceptors’. C-fibres cause slower, poorly localized pain.
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C-fibres have small diameter, unmyelinated axons with free nerve endings ( Rang et al 1991, Woolf 1991) associated with polymodal nociceptors which can be stimulated by thermal, mechanical or chemical stimuli. Stimulation of A-delta fibres results in sharp, well-localized pain felt almost immediately ( Davies & Blakeley 2001). A-delta fibres tend to be associated with mechanical and thermal nociceptors (Holdcroft 2005) and respond to one stimulus only (unimodal). Nociceptive neurons are divided into A-delta fibres (20%) and C-fibres (80%). A-beta fibres are low-threshold, cutaneous mechanoreceptors.
A-alpha fibres innervate muscle spindles and golgi tendon organs and their main function is proprioception (Chapter 6.4). Table 3.2 The classification of nerve fibresĪ-fibres have large cell body diameters and are divided into three subgroups: A-alpha, A-beta and A-delta fibres. Sensitization, recruitment of silent nociceptors, alteration in phenotype, hyperinnervationĬentral sensitization and recruitment, summation, amplificationĪcquisition of spontaneous and stimulus evoked activity by nociceptor axons at loci other than peripheral terminals, phenotype changeĬentral sensitization, deafferentation of second-order neurons, disinhibition and structural reorganization Transient pain (response to noxious stimulus with no long-term effect e.g. Table 3.1 A mechanism-based classification system for pain (Woolf 1998) Sensitization of the peripheral and central nervous system are the underlying mechanisms for these signs (Table 3.1).
Hyperalgesia is an exaggerated pain response to a noxious stimulus, while allodynia is a pain response produced by a non-noxious stimulus.
Common signs are hyperalgesia and allodynia.
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