Forebrain overexpression of CaMKII abolishes cingulate long term depression and reduces mechanical allodynia and thermal hyperalgesia
<p>Abstract</p> <p>Activity-dependent synaptic plasticity is known to be important in learning and memory, persistent pain and drug addiction. Glutamate NMDA receptor activation stimulates several protein kinases, which then trigger biochemical cascades that lead to modifications i...
Main Authors: | Tsien Joe Z, Wang Huimin, Shokat Kevan M, Zhang Chao, Wang Guo-Du, Wei Feng, Liauw Jason, Zhuo Min |
---|---|
Format: | Article |
Language: | English |
Published: |
SAGE Publishing
2006-06-01
|
Series: | Molecular Pain |
Online Access: | http://www.molecularpain.com/content/2/1/21 |
Similar Items
-
Protection of α-CaMKII from Dephosphorylation by GluN2B Subunit of NMDA Receptor Is Abolished by Mutation of Glu96 or His282 of α-CaMKII.
by: Madhavan Mayadevi, et al.
Published: (2016-01-01) -
Allodynia and hyperalgesia: review
by: K. D. Dmytriiev, et al.
Published: (2018-09-01) -
The role and mechanism of esketamine in preventing and treating remifentanil-induced hyperalgesia based on the NMDA receptor–CaMKII pathway
by: Wang Jiafang, et al.
Published: (2024-01-01) -
Mechanisms of CaMKII Activation
by: Jeffrey R Erickson
Published: (2014-04-01) -
The role of calcium and CaMKII in sleep
by: Yuyang Wang, et al.
Published: (2022-12-01)