 |
|||||
|
|||||
|
|||||
|
|||||
|
|||||
Previous Article | Next Article
The Journal of Neuroscience, May 15, 2002, 22(10):4196-4204
Calcium-Calmodulin-Dependent Protein Kinase II Contributes to Spinal Cord Central Sensitization
Li Fang*, Jing Wu*, Qing Lin, and William D. Willis Department of Anatomy and Neurosciences, Marine Biomedical Institute, The University of Texas Medical Branch, Galveston, Texas 77555-1069
Calcium/calmodulin-dependent protein kinase II (CaMK II) is found throughout the CNS. It regulates calcium signaling in synaptic transmission by phosphorylating various proteins, including neuronal membrane receptors and intracellular transcription factors. Inflammation or injuries to peripheral tissues cause long-lasting increases in the responses of central nociceptive neurons to innocuous and noxious stimuli. This change can occur independently of alterations in the responsiveness of primary afferent neurons and has been termed central sensitization. Central sensitization is a form of activity-dependent plasticity and results from interactions in a set of intracellular signaling pathways, which modulate nociceptive transmission. Here we demonstrate an increased expression and phosphorylation of CaMK II in rat spinal dorsal horn neurons after noxious stimulation by intradermal injection of capsaicin. Local administration of a CaMK II inhibitor in the spinal cord significantly inhibits the enhancement of responses of spinal nociceptive neurons and changes in exploratory behavior evoked by capsaicin injection. In addition, spinal CaMK II activity enhances phosphorylation of AMPA receptor GluR1 subunits during central sensitization produced by capsaicin injection. This study reveals that CaMK II contributes to central sensitization in a manner similar to its role in the processes underlying long-term potentiation.
Key words: CaMK II; central sensitization; long-term potentiation; protein phosphorylation; intradermal capsaicin injection; spinal cord
* L.F. and J.W. contributed equally to this work.
Copyright © 2002 Society for Neuroscience 0270-6474/02/22104196-09$05.00/0
This article has been cited by other articles:
J. Sandkuhler
Models and Mechanisms of Hyperalgesia and Allodynia
Physiol Rev, April 1, 2009; 89(2): 707 - 758.
[Abstract] [Full Text] [PDF]
M. Larsson and J. Broman
Translocation of GluR1-Containing AMPA Receptors to a Spinal Nociceptive Synapse during Acute Noxious Stimulation
J. Neurosci., July 9, 2008; 28(28): 7084 - 7090.
[Abstract] [Full Text] [PDF]
S. Pezet, F. Marchand, R. D'Mello, J. Grist, A. K. Clark, M. Malcangio, A. H. Dickenson, R. J. Williams, and S. B. McMahon
Phosphatidylinositol 3-Kinase Is a Key Mediator of Central Sensitization in Painful Inflammatory Conditions
J. Neurosci., April 16, 2008; 28(16): 4261 - 4270.
[Abstract] [Full Text] [PDF]
F. Luo, C. Yang, Y. Chen, P. Shukla, L. Tang, L. X. Wang, and Z. J. Wang
Reversal of Chronic Inflammatory Pain by Acute Inhibition of Ca2+/Calmodulin-Dependent Protein Kinase II
J. Pharmacol. Exp. Ther., April 1, 2008; 325(1): 267 - 275.
[Abstract] [Full Text] [PDF]
T. L. Jones, A. C. Lustig, and L. S. Sorkin
Secondary Hyperalgesia in the Postoperative Pain Model Is Dependent on Spinal Calcium/Calmodulin-Dependent Protein Kinase II{alpha} Activation
Anesth. Analg., December 1, 2007; 105(6): 1650 - 1656.
[Abstract] [Full Text] [PDF]
T. Klein, W. Magerl, and R.-D. Treede
Perceptual Correlate of Nociceptive Long-Term Potentiation (LTP) in Humans Shares the Time Course of Early-LTP
J Neurophysiol, December 1, 2006; 96(6): 3551 - 3555.
[Abstract] [Full Text] [PDF]
S. Valencia-de Ita, N. B. Lawand, Q. Lin, G. Castaneda-Hernandez, and W. D. Willis
Role of the Na+-K+-2Cl- Cotransporter in the Development of Capsaicin-Induced Neurogenic Inflammation
J Neurophysiol, June 1, 2006; 95(6): 3553 - 3561.
[Abstract] [Full Text] [PDF]
M. Larsson and J. Broman
Pathway-specific bidirectional regulation of Ca2+/calmodulin-dependent protein kinase II at spinal nociceptive synapses after acute noxious stimulation.
J. Neurosci., April 19, 2006; 26(16): 4198 - 4205.
[Abstract] [Full Text] [PDF]
T. K. Pareek, J. Keller, S. Kesavapany, H. C. Pant, M. J. Iadarola, R. O. Brady, and A. B. Kulkarni
Cyclin-dependent kinase 5 activity regulates pain signaling
PNAS, January 17, 2006; 103(3): 791 - 796.
[Abstract] [Full Text] [PDF]
Y. Kawasaki, T. Kohno, Z.-Y. Zhuang, G. J. Brenner, H. Wang, C. Van Der Meer, K. Befort, C. J. Woolf, and R.-R. Ji
Ionotropic and Metabotropic Receptors, Protein Kinase A, Protein Kinase C, and Src Contribute to C-Fiber-Induced ERK Activation and cAMP Response Element-Binding Protein Phosphorylation in Dorsal Horn Neurons, Leading to Central Sensitization
J. Neurosci., September 22, 2004; 24(38): 8310 - 8321.
[Abstract] [Full Text] [PDF]
G.-Y. Xu and L.-Y. M. Huang
Ca2+/calmodulin-dependent protein kinase II potentiates ATP responses by promoting trafficking of P2X receptors
PNAS, August 10, 2004; 101(32): 11868 - 11873.
[Abstract] [Full Text] [PDF]
T. L. Jones and L. S. Sorkin
Calcium-Permeable {alpha}-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid/Kainate Receptors Mediate Development, but Not Maintenance, of Secondary Allodynia Evoked by First-Degree Burn in the Rat
J. Pharmacol. Exp. Ther., July 1, 2004; 310(1): 223 - 229.
[Abstract] [Full Text] [PDF]
H.-W. Yang, X.-D. Hu, H.-M. Zhang, W.-J. Xin, M.-T. Li, T. Zhang, L.-J. Zhou, and X.-G. Liu
Roles of CaMKII, PKA, and PKC in the Induction and Maintenance of LTP of C-Fiber-Evoked Field Potentials in Rat Spinal Dorsal Horn
J Neurophysiol, March 1, 2004; 91(3): 1122 - 1133.
[Abstract] [Full Text] [PDF]
A. B. Petrenko, T. Yamakura, H. Baba, and K. Shimoji
The Role of N-Methyl-D-Aspartate (NMDA) Receptors in Pain: A Review
Anesth. Analg., October 1, 2003; 97(4): 1108 - 1116.
[Abstract] [Full Text] [PDF]
H. Ikeda, B. Heinke, R. Ruscheweyh, and J. Sandkuhler
Synaptic Plasticity in Spinal Lamina I Projection Neurons That Mediate Hyperalgesia
Science, February 21, 2003; 299(5610): 1237 - 1240.
[Abstract] [Full Text] [PDF]
|
|
|
|
 |
|