| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
ARTICLES |
W. M. Keck Foundation Center for Integrative Neuroscience (B.K.T., M.A.P., A.I.B.) and Departments of Anatomy (B.K.T., M.A.P., A.I.B.) and Physiology (S.F.A., M.F.D., A.I.B.), University of California, San Francisco, San Francisco, California 94143-0452
Address all correspondence and requests for reprints to: Brad Taylor, Ph.D., Assistant Research Professor, Department of Anatomy, University of California, San Francisco, Box 0452, San Francisco, California 94143-0452. E-mail: brad{at}phy.ucsf.edu
Although glucocorticoids inhibit inflammation and are used to treat painful inflammatory rheumatic diseases, the contribution, if any, of endogenous pituitary-adrenocortical activity to the control of pain remains unclear. We report that injection of dilute formalin into the hindpaw not only evokes inflammation and pain-related behavior, but it also increases ACTH and corticosterone to a greater extent than restraint and saline injection alone. This difference was particularly robust during the final periods of pain-related behavior in the formalin test, when the ACTH and corticosterone (B) levels in the restraint/saline control group had returned to normal. These results indicate that formalin-evoked increases in ACTH and B reflect nociceptive input, rather than the stress associated with handling. To test the hypothesis that the formalin-induced increase in corticosterone reduces pain and inflammation, we next evaluated the effect of adrenalectomy (to prevent activation of glucocorticoid receptors) or high-dose dexamethasone (to saturate glucocorticoid receptors) on nociceptive processing in the formalin test. Neither adrenalectomy nor dexamethasone changed behavioral or cardiovascular nociceptive responses. Furthermore, the increases in blood pressure and heart rate produced by formalin may not be mediated by adrenomedullary catecholamine release. In addition, we conclude that the nociceptive component of the formalin stimulus is sufficient to activate the pituitary-adrenocortical system in the awake rat, but that the resulting release of corticosterone does not feed back and reduce nociceptive processing.
This article has been cited by other articles:
 |
|
 |
|
  K. Vissers, H. Adriaensen, R. De Coster, C. De Deyne, and T. F. Meert A Chronic-Constriction Injury of the Sciatic Nerve Reduces Bilaterally the Responsiveness to Formalin in Rats: A Behavioral and Hormonal Evaluation Anesth. Analg., August 1, 2003; 97(2): 520 - 525. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Le Bars, M. Gozariu, and S. W. Cadden Animal Models of Nociception Pharmacol. Rev., December 1, 2001; 53(4): 597 - 652. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Pacak and M. Palkovits Stressor Specificity of Central Neuroendocrine Responses: Implications for Stress-Related Disorders Endocr. Rev., August 1, 2001; 22(4): 502 - 548. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. L. Yaksh, G. Ozaki, D. McCumber, M. Rathbun, C. Svensson, S. Malkmus, and M. C. Yaksh An automated flinch detecting system for use in the formalin nociceptive bioassay J Appl Physiol, June 1, 2001; 90(6): 2386 - 2402. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Piva, G. M. Horowitz, and K. L. Sharpe-Timms Interleukin-6 Differentially Stimulates Haptoglobin Production by Peritoneal and Endometriotic Cells in Vitro: A Model for Endometrial-Peritoneal Interaction in Endometriosis J. Clin. Endocrinol. Metab., June 1, 2001; 86(6): 2553 - 2561. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |
