JPET Assistant Professor of Medicine (Clinician-Educator)

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
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 Sluka, K. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sluka, K. A.

Vol. 287, Issue 1, 232-237, October 1998

Blockade of N- and P/Q-Type Calcium Channels Reduces the Secondary Heat Hyperalgesia Induced by Acute Inflammation

K. A. Sluka

Physical Therapy Graduate Program, Neuroscience Graduate Program, University of Iowa, Iowa City, Iowa

High voltage calcium channels are implicated in nociceptive transmission after nerve injury, capsaicin or formalin injection. The purpose of this study was to investigate the role of calcium channels in secondary heat hyperalgesia associated with acute joint inflammation. After induction of acute inflammation (knee joint injection of kaolin and carrageenan), decreased paw withdrawal latency (PWL) to radiant heat (i.e., secondary heat hyperalgesia), increased guarding of the limb and increased joint circumference occurs. Spinal administration (through a microdialysis fiber placed in dorsal horn) of an N-type calcium channel blocker (MVIIA, SNX 111, ziconotide, 0.001-0.1 mM), before induction of inflammation, prevents the decrease in PWL. Treatment with SNX 111 4 hr after inflammation reverses heat hyperalgesia. A small reduction in spontaneous pain-related behaviors (guarding of the limb) occurs after pre- or post-treatment with SNX 111. Spinal blockade of P/Q-type calcium channels (with omega -agatoxin IVA) had no effect on the decrease in PWL to radiant heat when administered after induction of inflammation. However, pre-treatment with omega -agatoxin IVA prevents secondary heat hyperalgesia. omega -Agatoxin IVA has no effect on spontaneous pain-related behaviors whether administered before or after induction of inflammation. In contrast, pre or post-treatment with nifedipine (L-type calcium channel blocker, 0.01-1.0 mM), had no effect on heat hyperalgesia or spontaneous pain-related behaviors induced by acute inflammation. There were no differences in joint circumference between groups with any treatment. Thus, N-type calcium channels contribute to both the development and maintenance of secondary heat hyperalgesia while P-type calcium channels are only involved during development of hyperalgesia.

0022-3565/98/2871-0232$03.00/0
THE JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
Copyright © 1998 by The American Society for Pharmacology and Experimental Therapeutics


This article has been cited by other articles:


Home page
 Anesth. Analg.Home page
Q. Hogan, P. Lirk, M. Poroli, M. Rigaud, A. Fuchs, P. Fillip, M. Ljubkovic, G. Gemes, and D. Sapunar
Restoration of Calcium Influx Corrects Membrane Hyperexcitability in Injured Rat Dorsal Root Ganglion Neurons
Anesth. Analg., September 1, 2008; 107(3): 1045 - 1051.
[Abstract] [Full Text] [PDF]

Home page
 J. Physiol.Home page
K. Nurgali, T. V. Nguyen, H. Matsuyama, M. Thacker, H. L. Robbins, and J. B. Furness
Phenotypic changes of morphologically identified guinea-pig myenteric neurons following intestinal inflammation
J. Physiol., September 1, 2007; 583(2): 593 - 609.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
C. Altier, C. S. Dale, A. E. Kisilevsky, K. Chapman, A. J. Castiglioni, E. A. Matthews, R. M. Evans, A. H. Dickenson, D. Lipscombe, N. Vergnolle, et al.
Differential Role of N-Type Calcium Channel Splice Isoforms in Pain
J. Neurosci., June 13, 2007; 27(24): 6363 - 6373.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
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]

Home page
 J. Pharmacol. Exp. Ther.Home page
R. Radhakrishnan and K. A. Sluka
Acetazolamide, a Carbonic Anhydrase Inhibitor, Reverses Inflammation-Induced Thermal Hyperalgesia in Rats
J. Pharmacol. Exp. Ther., May 1, 2005; 313(2): 921 - 927.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurophysiol.Home page
J. Nebe, A. Ebersberger, H. Vanegas, and H.-G. Schaible
Effects of omega -Agatoxin IVA, a P-Type Calcium Channel Antagonist, on the Development of Spinal Neuronal Hyperexcitability Caused by Knee Inflammation in Rats
J Neurophysiol, June 1, 1999; 81(6): 2620 - 2626.
[Abstract] [Full Text] [PDF]


Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
All ASPET Journals Molecular Pharmacology Pharmacological Reviews
Molecular Interventions Drug Metabolism and Disposition

Copyright © 1998 by the American Society for Pharmacology and Experimental Therapeutics.