Effects of Corticotropin-Releasing Factor (CRF) on Somatic Pain Sensitivity in Conscious Rats: Involvement of Types 1 and 2 CRF Receptors

Corticotrophin-releasing factor (CRF) is involved in regulating pain sensitivity and can elicit analgesic effects in animals and humans. The aim of the present work was to investigate the involvement of types 1 and 2 CRF receptors (CRF-1 and CRF-2 receptors) in mediating the analgesic action of CRF...

Full description

Saved in:
Bibliographic Details
Published inNeuroscience and behavioral physiology Vol. 46; no. 4; pp. 472 - 477
Main Authors Yarushkina, N. I., Bagaeva, T. R., Filaretova, L. P.
Format Journal Article
LanguageEnglish
Published New York Springer US 01.05.2016
Springer Nature B.V
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Corticotrophin-releasing factor (CRF) is involved in regulating pain sensitivity and can elicit analgesic effects in animals and humans. The aim of the present work was to investigate the involvement of types 1 and 2 CRF receptors (CRF-1 and CRF-2 receptors) in mediating the analgesic action of CRF on somatic pain sensitivity when given systemically to conscious rats. Somatic pain sensitivity was tested in terms of the latent period (LP) of the tailflick reaction in response to thermal stimulation (the tail flick test). The involvement of CRF-1 and CFR-2 receptors was studied by systemic administration of their specific antagonists NBI 27914 and astressin 2B, respectively. Systemic administration of CRF increased the latent period of the pain reaction (it had an analgesic effect). Prior administration of NBI 27914 or astressin 2B eliminated the analgesic effect of CRF. In addition, administration of NBI 27914 affected the basal latent period of the pain reaction, increasing it. These data provide evidence that the analgesic effect of CRF may be mediated by both CRF-1 and CRF-2 receptors. CRF-1 receptors, unlike CRF-2 receptors, may also be involved in regulating the basal level of pain sensitivity.
ISSN:0097-0549
1573-899X
DOI:10.1007/s11055-016-0260-7