The potentiating effect of calcitonin gene-related peptide on transient receptor potential vanilloid-1 activity and the electrophysiological responses of rat trigeminal neurons to nociceptive stimuli

Growing evidence suggests that calcitonin gene-related peptide (CGRP) participates in trigeminal nociceptive responses. However, the role of CGRP in sensitization or desensitization of nociceptive transduction remains poorly understood. In this study, we sought to further investigate the CGRP-induce...

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Bibliographic Details
Published in:The journal of physiological sciences 2018-05, Vol.68 (3), p.261-268
Main Authors: Chatchaisak, Duangthip, Connor, Mark, Srikiatkhachorn, Anan, Chetsawang, Banthit
Format: Article
Language:English
Subjects:
Animals
Ca2+/calmodulin-dependent protein kinase II
Calcitonin
Calcitonin gene-related peptide
Calcitonin Gene-Related Peptide - pharmacology
Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism
Capsaicin
Capsaicin receptors
Cyclic AMP-Dependent Protein Kinases - antagonists & inhibitors
Electrophysiological Phenomena - drug effects
Enzyme inhibitors
Genes
Isoquinolines - pharmacology
Kinases
Male
Neurons
Neurons - drug effects
Neurons - metabolism
Nociceptors - metabolism
Original Paper
Pain perception
Peptides
Protein kinase A
Protein kinases
Rats
Rats, Wistar
Sulfonamides - pharmacology
Transient receptor potential proteins
Trigeminal ganglion
Trigeminal Ganglion - drug effects
Trigeminal Ganglion - metabolism
TRPV Cation Channels - metabolism
Up-Regulation - drug effects
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Summary:Growing evidence suggests that calcitonin gene-related peptide (CGRP) participates in trigeminal nociceptive responses. However, the role of CGRP in sensitization or desensitization of nociceptive transduction remains poorly understood. In this study, we sought to further investigate the CGRP-induced up-regulation of transient receptor potential vanilloid-1 (TRPV1) and the responses of trigeminal neurons to nociceptive stimuli. Rat trigeminal ganglion (TG) organ cultures and isolated trigeminal neurons were incubated with CGRP. An increase in TRPV1 levels was observed in CGRP-incubated TG organ cultures. CGRP potentiated capsaicin-induced increase in phosphorylated CaMKII levels in the TG organ cultures. The incubation of the trigeminal neurons with CGRP significantly increased the inward currents in response to capsaicin challenge, and this effect was inhibited by co-incubation with the CGRP receptor antagonist, BIBN4068BS or the inhibitor of protein kinase A, H-89. These findings reveal that CGRP acting on trigeminal neurons may play a significant role in facilitating cellular events that contribute to the peripheral sensitization of the TG in nociceptive transmission.
ISSN:1880-6546
1880-6562
DOI:10.1007/s12576-017-0529-9