Home Subscription Services
 
   

 
Journal of Oral & Facial Pain and Headache
OFPH Home Page
About the Editor
Editorial Board
Accepted Manuscripts
Submit
Author Guidelines
Submission Form
Reprints / Articles
Permissions
Advertising
MEDLINE Search
 
 
 
 
 
FacebookTwitterYouTube
Quintessence Publishing: Journals: OFPH
Journal of Oral & Facial Pain and Headache

Edited by Barry J. Sessle, BDS, MDS, BSc, PhD, FRSC

Official Journal of the American Academy of Orofacial Pain,
the European, Asian, and Ibero-Latin Academies of Craniomandibular
Disorders, and the Australian Academy of Orofacial Pain

ISSN 2333-0384 (print) • ISSN 2333-0376 (online)

Publication:
Fall 2004
Volume 18 , Issue 4

Back
Share Abstract:

Cellular Neuroplasticity Mechanisms Mediating Pain Persistence

Michael W. Salter, MD, PhD

Pages: 318 - 324
PMID: 15636015

Transmission of noxious-stimulus-evoked inputs in the spinal and trigeminal systems is mediated primarily through excitatory glutamatergic synapses using alpha amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA), kainate and N-methyl-D-aspartate (NMDA) subtypes of glutamate receptors. Glutamatergic synapses exhibit multiple forms of short-lasting and long-lasting synaptic plasticity. Persistent enhancement of nociceptive transmission, known as “central sensitization,” is a form of lasting plasticity that is similar mechanistically to long-term potentiation of glutamatergic transmission in other regions of the central nervous system. This potentiation of AMPA/kainate transmission is dependent upon the activity of NMDA receptors, which become enhanced following noxious peripheral stimulation as a result of several convergent mechanisms. Central sensitization is thus an expression of increased synaptic gain at glutamatergic synapses in central nociceptive-transmission neurons and thereby contributes importantly to pain hypersensitivity. In addition, recent evidence has revealed a new player in the mechanisms underlying pain hypersensitivity following nerve injury—microglia. Understanding of the roles of microglia may lead to new strategies for the diagnosis and management of neuropathic pain.

Full Text PDF File | Order Article

 

 
Get Adobe Reader
Adobe Acrobat Reader is required to view PDF files. This is a free program available from the Adobe web site.
Follow the download directions on the Adobe web site to get your copy of Adobe Acrobat Reader.
  © 2014 Quintessence Publishing Co Inc
 

Home | Subscription Services | Books | Journals | Multimedia | Events | Blog
Terms of Use | Privacy Policy | About Us | Contact Us | Advertising | Help | Sitemap | Catalog