scholarly journals Dorsal Horn α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid Receptor Trafficking in Inflammatory Pain

2010 ◽  
Vol 112 (5) ◽  
pp. 1259-1265 ◽  
Author(s):  
Yuan-Xiang Tao ◽  
David S. Warner
Keyword(s):  
Dorsal Horn ◽  
Aspartic Acid ◽  
Central Sensitization ◽  
Inflammatory Pain ◽  
Persistent Pain ◽  
Receptor Trafficking ◽  
Current Evidence ◽  
Receptor Subunit ◽  
Acid Receptor ◽  
Dorsal Horn Neurons

Activation of synaptic N-methyl-D-aspartic acid receptor and its intracellular downstream signals in dorsal horn neurons of spinal cord contribute to central sensitization, a mechanism that underlies the development and maintenance of pain hypersensitivity in persistent pain. However, the molecular process of this event is not understood completely. Recently, new studies suggest that peripheral inflammatory insults drive changes in alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor subunit trafficking via N-methyl-D-aspartic acid receptor-triggered activation of protein kinases in dorsal horn and raise the possibility that such changes might contribute to central sensitization in persistent pain. This review presents current evidence regarding the changes that occur in the trafficking of dorsal horn alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor subunits GluR1 and GluR2 under persistent inflammatory pain conditions and discusses the potential mechanisms by which such changes participate in the development and maintenance of inflammatory pain.

scholarly journals Peripheral and central hyperexcitability: Differential signs and symptoms in persistent pain

1997 ◽  
Vol 20 (3) ◽  
pp. 404-419 ◽  
Author(s):  
Terence J. Coderre ◽  
Joel Katz
Keyword(s):  
Neuropathic Pain ◽  
Postoperative Pain ◽  
Experimental Evidence ◽  
Dorsal Horn ◽  
Central Sensitization ◽  
Signs And Symptoms ◽  
Persistent Pain ◽  
Dorsal Horn Neurons ◽  
Target Article

This target article examines the clinical and experimental evidence for a role of peripheral and central hyperexcitability in persistent pain in four key areas: cutaneous hyperalgesia, referred pain, neuropathic pain, and postoperative pain. Each suggests that persistent pain depends not only on central sensitization, but also on inputs from damaged peripheral tissue. It is instructive to think of central sensitization as comprised of both an initial central sensitization and an ongoing central sensitization driven by inputs from peripheral sources. Each of these factors, initial sensitization, ongoing central sensitization, and inputs from peripheral sources, contributes to the net activity in dorsal horn neurons and thus influences the expression of persistent pain or hyperalgesia. Since each factor, peripheral inputs and central sensitization (initial or ongoing), can contribute to both the initiation and maintenance of persistent pain, therapies should target both peripheral and central sources of pathology.

scholarly journals Effect of Ginkgo Biloba Extract on N-Methyl-D-Aspartic Acid Receptor Subunit 2B Expression in a Salicylate-Induced Ototoxicity Model

2019 ◽  
Vol 12 (2) ◽  
pp. 169-175
Author(s):  
Sang-Yeon Lee ◽  
Sang Yoon Han ◽  
Ye-Ji Shim ◽  
Jae-Joon Han ◽  
DeukTae Cho ◽  
...  
Keyword(s):  
Aspartic Acid ◽  
Ginkgo Biloba ◽  
Ginkgo Biloba Extract ◽  
Receptor Subunit ◽  
Acid Receptor

Fentanyl Enhancement of Carrageenan-induced Long-lasting Hyperalgesia in Rats

2002 ◽  
Vol 96 (2) ◽  
pp. 381-391 ◽  
Author(s):  
Cyril Rivat ◽  
Jean-Paul Laulin ◽  
Jean-Benoît Corcuff ◽  
Evelyne Célèrier ◽  
Laure Pain ◽  
...  
Keyword(s):  
Tissue Damage ◽  
Central Sensitization ◽  
Inflammatory Pain ◽  
Pain Sensitivity ◽  
Persistent Pain ◽  
The Other ◽  
Carrageenan Injection ◽  
Opiate Treatment

Background Tissue damage may produce hyperalgesia, allodynia, and persistent pain. The authors recently reported that fentanyl elicits analgesia but also activates N-methyl-D-aspartate-dependent pain facilitatory processes opposing analgesia. In nonsuffering rats, this leads to a long-lasting enhancement in pain sensitivity. The current study assessed whether fentanyl could amplify carrageenan-induced hyperalgesia. Methods First, rats were injected once with carrageenan in a hind paw, with fentanyl (60 or 100 microg/kg each given four times at 15-min intervals [4 x 60 or 4 x100]) or saline. Second, rats were injected with carrageenan twice without fentanyl (7-day interval), with the second injection either in the previously injected paw or in the other paw. Third, rats were injected twice with carrageenan in the same hind paw: the first ketamine injection was given (10 mg/kg each given three times at 5-h intervals) with or without fentanyl (4 x 60 microg/kg), and second injection was given without ketamine or fentanyl. The consequences of treatments on long-term hyperalgesia were examined by the paw-pressure vocalization test. Results The long-lasting hyperalgesia induced by the first carrageenan injection was dose-dependently enhanced in both duration and magnitude in 4 x 60 or 4 x 100 microg/kg fentanyl-treated rats: 5 or 10 days, respectively, as compared with 2 days in saline-treated rats. Hyperalgesia observed in the hind paw contralateral to the first carrageenan injection was enhanced in fentanyl-treated rats. The second carrageenan injection, performed in any hind paw, induced an exaggerated hyperalgesia, especially in fentanyl-treated rats. Pretreatment with ketamine totally prevented the carrageenan- and fentanyl-induced enhancement of the long-lasting hyperalgesia. Conclusion Central sensitization in inflammatory pain states is reinforced by an opiate treatment, which could be prevented by N-methyl-D-aspartate receptors blockade.

Sign in / Sign up

Export Citation Format

Share Document