LOGIN TO YOUR ACCOUNT

Username
Password
Remember Me
Or use your Academic/Social account:

CREATE AN ACCOUNT

Or use your Academic/Social account:

Congratulations!

You have just completed your registration at OpenAire.

Before you can login to the site, you will need to activate your account. An e-mail will be sent to you with the proper instructions.

Important!

Please note that this site is currently undergoing Beta testing.
Any new content you create is not guaranteed to be present to the final version of the site upon release.

Thank you for your patience,
OpenAire Dev Team.

Close This Message

CREATE AN ACCOUNT

Name:
Username:
Password:
Verify Password:
E-mail:
Verify E-mail:
*All Fields Are Required.
Please Verify You Are Human:
fbtwitterlinkedinvimeoflicker grey 14rssslideshare1
Drake, Robert A.R.; Leith, J.L.; Almahasneh, F.; Martindale, J.; Wilson, A.W.; Lumb, B.M.; Donaldson, Lucy F. (2016)
Publisher: Society for Neuroscience
Languages: English
Types: Article
Subjects: Periaqueductal Grey, /dk/atira/pure/researchoutput/pubmedpublicationtype/D016428, /dk/atira/pure/researchoutput/pubmedpublicationtype/D013485, Arthritis, A-nociceptors, Descending Facilitation, Prostaglandins, Journal Article, Secondary hyperalgesia, Articles, Research Support, Non-U.S. Gov't

Classified by OpenAIRE into

mesheuropmc: nervous system
Descending controls on spinal nociceptive processing play a pivotal role in shaping the pain experience following tissue injury. Secondary hypersensitivity develops within undamaged tissue adjacent, and distant to, damaged sites. Spinal neuronal pools innervating regions of secondary hypersensitivity are dominated by descending facilitation that amplifies spinal inputs from un-sensitized peripheral nociceptors. Cyclooxygenase–prostaglandin E2 signaling within the ventrolateral periaqueductal grey (vlPAG) is pro-nociceptive in naïve and acutely inflamed animals but its contributions in more prolonged inflammation and, importantly, secondary hypersensitivity remain unknown. In naïve rats, prostaglandin EP3 receptor (EP3R) antagonism in vlPAG modulated noxious withdrawal reflex (EMG) thresholds to preferential C-, but not A-, nociceptor activation, and raised thermal withdrawal thresholds in awake animals. In rats with inflammatory arthritis, secondary mechanical and thermal hypersensitivity of the hind-paw developed, and this was associated with spinal sensitization to Anociceptor inputs alone. In arthritic rats, blockade of vlPAG EP3R raised EMG thresholds to C-nociceptor activation in the area of secondary hypersensitivity to a degree equivalent to that evoked by the same manipulation in naïve rats. Importantly, vlPAG EP3R blockade also affected responses to A-nociceptor activation, but only in arthritic animals. We conclude that vlPAG EP3R activity exerts an equivalent facilitation on the spinal processing of C-nociceptor inputs in naïve and arthritic animals but gains in effects on spinal A-nociceptor processing from a region of secondary hypersensitivity. Thus the spinal sensitization to A-nociceptor inputs associated with secondary hypersensitivity is likely to be, at least partly, dependent on descending prostanergic facilitation from the vlPAG.

Share - Bookmark

Funded by projects

  • WT | Functional anatomical studie...
  • RCUK | Local translation of mRNA ...

Cite this article