JN AJP: Endocrinology and Metabolism
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 QUICK SEARCH:   [advanced]


     


J Neurophysiol (June 7, 2006). doi:10.1152/jn.00495.2006
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
96/4/1803    most recent
00495.2006v2
00495.2006v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Li, W.
Right arrow Articles by Neugebauer, V. E
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Li, W.
Right arrow Articles by Neugebauer, V. E
Submitted on May 9, 2006
Accepted on May 31, 2006

Differential changes of group II and group III mGluR function in central amygdala neurons in a model of arthritic pain

Weidong Li1 and Volker E Neugebauer1*

1 Neuroscience and Cell Biology, University of Texas Medical Branch, Galveston, Texas, United States

* To whom correspondence should be addressed. E-mail: voneugeb{at}utmb.edu.

Metabotropic glutamate receptors (mGluRs) play important roles in neuroplasticity and disorders such as persistent pain. Group I mGluRs contribute to pain-related sensitization and synaptic plasticity of neurons in the laterocapsular division of the central nucleus of the amygdala (CeLC), but the roles of groups II and III mGluRs are not known. Extracellular single-unit recordings were made from 60 CeLC neurons in anesthetized adult rats. Background activity and evoked responses were measured before and during the development of the kaolin/carrageenan-induced knee joint arthritis. Drugs were administered into the CeLC by microdialysis before and/or after arthritis induction. A selective group III mGluR agonist (LAP4) inhibited CeLC neurons' responses to stimulation of the knee and ankle in arthritis (n=7) more potently than under normal conditions (n=14). A selective group II agonist (LY354740) inhibited responses under normal conditions (n=12) and became more potent in inhibiting responses to noxious stimulation of the knee in arthritis (n=10). The effect of LY354740 on innocuous stimulation of the knee and stimulation of the ankle did not change in arthritis. Antagonists for group II (EGLU, n=9) and III (UBP1112, n=8) had no effects under normal conditions. In arthritis, UPB1112 (n=5) facilitated the responses to stimulation of knee and ankle whereas EGLU (n=5) selectively increased the responses to stimulation of the knee. These data suggest that group II and III mGluRs inhibit nociceptive processing in CeLC neurons. The increased function and endogenous activation of group II mGluRs in arthritis appear more input-selective than the general changes of group III mGluRs.




This article has been cited by other articles:


Home page
J. Neurophysiol.Home page
G. Ji and V. Neugebauer
Hemispheric Lateralization of Pain Processing by Amygdala Neurons
J Neurophysiol, October 1, 2009; 102(4): 2253 - 2264.
[Abstract] [Full Text] [PDF]


Home page
J. Neurosci.Home page
Y. Fu and V. Neugebauer
Differential Mechanisms of CRF1 and CRF2 Receptor Functions in the Amygdala in Pain-Related Synaptic Facilitation and Behavior
J. Neurosci., April 9, 2008; 28(15): 3861 - 3876.
[Abstract] [Full Text] [PDF]


Home page
J. Neurophysiol.Home page
G. Ji and V. Neugebauer
Pro- and Anti-Nociceptive Effects of Corticotropin-Releasing Factor (CRF) in Central Amygdala Neurons Are Mediated Through Different Receptors
J Neurophysiol, March 1, 2008; 99(3): 1201 - 1212.
[Abstract] [Full Text] [PDF]


Home page
J. Neurophysiol.Home page
G. Ji and V. Neugebauer
Differential Effects of CRF1 and CRF2 Receptor Antagonists on Pain-Related Sensitization of Neurons in the Central Nucleus of the Amygdala
J Neurophysiol, June 1, 2007; 97(6): 3893 - 3904.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 2006 by the The American Physiological Society.