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2023, Handbook of Clinical NeurologyExpression pattern of type 3 adenylyl cyclase in rodent dorsal root ganglion and its primary afferent terminals
2019, Neuroscience LettersCitation Excerpt :CGRP release from its storage vesicles can be stimulated by neonatal capsaicin [23]. CGRP could potentiate substance P function in the spinal dorsal horn [24,25] as well as enhance release of substance P [26] and excitatory amino acids [27] from primary afferents. Furthermore, CGRP is released in the spinal cord following noxious mechanical, thermal or electrical stimulation [28].
Neuropeptides and ATP signaling in the trigeminal ganglion
2017, Japanese Dental Science ReviewA potent and selective calcitonin gene-related peptide (CGRP) receptor antagonist, MK-8825, inhibits responses to nociceptive trigeminal activation: Role of CGRP in orofacial pain
2015, Experimental NeurologyCitation Excerpt :It has recently been implicated in the pathophysiology of TMDs in chronic masticatory muscle pain within the primary afferent neurons (Dessem and Lovering, 2011; Kehl et al., 2000; Ohlen et al., 1987). Previously it was thought that CGRP release from primary afferents modulates pain transmission only through interactions with substance P and excitatory amino acids (Biella et al., 1991; Oku et al., 1987; Smullin et al., 1990), but it is now also thought to cause hyperalgesia and central sensitization independent of these mechanisms (Lian et al., 2010; Sun et al., 2003, 2004). In the trigeminovascular system CGRP release is involved in sensitizing the primary afferent neurons causing peripheral and central sensitization in craniofacial inflammatory, neuropathic and migraine pain (Cady et al., 2011; De Felice et al., 2010).
Sensory nerve fibers containing calcitonin gene-related peptide in gastrocnemius, latissimus dorsi and erector spinae muscles and thoracolumbar fascia in mice
2015, NeuroscienceCitation Excerpt :Likewise, intrathecal administration of both peptides facilitates the pain withdrawal reflex to an exaggerated and more prolonged extent than administration of either peptide alone (Woolf and Wiesenfeld-Hallin, 1986). CGRP enhances SP-mediated transmission in three ways: CGRP can potentiate release of SP, presumably by a presynaptic action (Oku et al., 1987); it can enhance excitability of neurons receiving nociceptive inputs, at least in part by potentiating the actions of SP itself (Biella et al., 1991; Seybold et al., 2003; Sun et al., 2004; Bird et al., 2006); and it can inhibit the degradation of SP, thereby prolonging its action (Le Greves et al., 1985). Plastic changes in peptidergic sensory nerves that supply muscle may contribute to chronic muscle pain.