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Fentanyl decreases discharges of C and A nociceptors to suprathreshold mechanical stimulation in chronic inflammation.
J Neurophysiol. 2012 Nov; 108(10):2827-36.JN

Abstract

An essential component of mechanical hyperalgesia resulting from tissue injury is an enhanced excitability of nociceptive neurons, termed mechanical sensitization. Local application of opioids to inflamed rat paws attenuates mechanical hyperalgesia and reduces electrical excitability of C-fiber nociceptors in acute injury. Here, we examined the effects of the opioid receptor agonist fentanyl on the mechanical coding properties of not only C- but also A-fiber nociceptors innervating the rat hind paw in a model of chronic pain, i.e., 4 days after Freund's complete adjuvant-induced inflammation. The peripheral mechanosensitive terminals of C-fibers (n = 143), A-fibers (n = 79), and low-threshold mechanoreceptors (n = 25) were characterized using the in vitro skin-nerve preparation from the saphenous nerve. Although mechanical activation thresholds were not changed, discharges to suprathreshold mechanical stimuli were elevated significantly in both A- and C-fiber nociceptors from inflamed tissue. In addition, the proportion of nociceptors as well as the frequency of spontaneous discharges in A (14% vs. 0%)- and C (28% vs. 8%)-fibers were increased in inflamed compared with normal tissue. Fentanyl inhibited responses to suprathreshold stimuli in a significantly higher proportion of not only C (36% vs. 7%)- but also A (41% vs. 8%)-fibers in inflamed tissue in a naloxone-reversible and concentration-dependent manner. Our results demonstrate that mechanical sensitization persists in chronic inflammation, in correlation with behavioral hyperalgesia. Opioid sensitivity of both A- and C-fibers is markedly augmented. This is consistent with an upregulation or enhanced functionality of opioid receptors located at the peripheral terminals of sensitized nociceptors.

Authors+Show Affiliations

Department of Anesthesiology and Critical Care Medicine, Freie Universität Berlin, Charité Campus Benjamin Franklin, Berlin, Germany. rabih.moshourab@charite.deNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22956796

Citation

Moshourab, Rabih, and Christoph Stein. "Fentanyl Decreases Discharges of C and a Nociceptors to Suprathreshold Mechanical Stimulation in Chronic Inflammation." Journal of Neurophysiology, vol. 108, no. 10, 2012, pp. 2827-36.
Moshourab R, Stein C. Fentanyl decreases discharges of C and A nociceptors to suprathreshold mechanical stimulation in chronic inflammation. J Neurophysiol. 2012;108(10):2827-36.
Moshourab, R., & Stein, C. (2012). Fentanyl decreases discharges of C and A nociceptors to suprathreshold mechanical stimulation in chronic inflammation. Journal of Neurophysiology, 108(10), 2827-36. https://doi.org/10.1152/jn.00082.2012
Moshourab R, Stein C. Fentanyl Decreases Discharges of C and a Nociceptors to Suprathreshold Mechanical Stimulation in Chronic Inflammation. J Neurophysiol. 2012;108(10):2827-36. PubMed PMID: 22956796.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Fentanyl decreases discharges of C and A nociceptors to suprathreshold mechanical stimulation in chronic inflammation. AU - Moshourab,Rabih, AU - Stein,Christoph, Y1 - 2012/09/05/ PY - 2012/9/8/entrez PY - 2012/9/8/pubmed PY - 2013/5/1/medline SP - 2827 EP - 36 JF - Journal of neurophysiology JO - J Neurophysiol VL - 108 IS - 10 N2 - An essential component of mechanical hyperalgesia resulting from tissue injury is an enhanced excitability of nociceptive neurons, termed mechanical sensitization. Local application of opioids to inflamed rat paws attenuates mechanical hyperalgesia and reduces electrical excitability of C-fiber nociceptors in acute injury. Here, we examined the effects of the opioid receptor agonist fentanyl on the mechanical coding properties of not only C- but also A-fiber nociceptors innervating the rat hind paw in a model of chronic pain, i.e., 4 days after Freund's complete adjuvant-induced inflammation. The peripheral mechanosensitive terminals of C-fibers (n = 143), A-fibers (n = 79), and low-threshold mechanoreceptors (n = 25) were characterized using the in vitro skin-nerve preparation from the saphenous nerve. Although mechanical activation thresholds were not changed, discharges to suprathreshold mechanical stimuli were elevated significantly in both A- and C-fiber nociceptors from inflamed tissue. In addition, the proportion of nociceptors as well as the frequency of spontaneous discharges in A (14% vs. 0%)- and C (28% vs. 8%)-fibers were increased in inflamed compared with normal tissue. Fentanyl inhibited responses to suprathreshold stimuli in a significantly higher proportion of not only C (36% vs. 7%)- but also A (41% vs. 8%)-fibers in inflamed tissue in a naloxone-reversible and concentration-dependent manner. Our results demonstrate that mechanical sensitization persists in chronic inflammation, in correlation with behavioral hyperalgesia. Opioid sensitivity of both A- and C-fibers is markedly augmented. This is consistent with an upregulation or enhanced functionality of opioid receptors located at the peripheral terminals of sensitized nociceptors. SN - 1522-1598 UR - https://www.unboundmedicine.com/medline/citation/22956796/Fentanyl_decreases_discharges_of_C_and_A_nociceptors_to_suprathreshold_mechanical_stimulation_in_chronic_inflammation_ L2 - https://journals.physiology.org/doi/10.1152/jn.00082.2012?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -