Mechanisms of activation of the pituitary-adrenal axis by tissue injury in the rat.
Abstract
To characterize the mechanisms of the pituitary-adrenal (P-A) response to tissue injury, rats were injected intramuscularly (IM) with turpentine. This resulted in marked elevations in the plasma concentrations of ACTH and corticosterone within the first hour after injection, which were attenuated by either total deafferentation of the medial basal hypothalamus (MBH) or neonatal capsaicin pretreatment. The plasma concentrations of corticosterone remained elevated for 18 h in the turpentine-injected rats, despite a return of ACTH toward control values (by 2-4 h). Bioactive concentrations of interleukin-6 (IL-6) in plasma rose markedly after turpentine, and its concentrations were significantly correlated with plasma corticosterone concentrations 4-8 h after turpentine. Pretreatment with IL-1 receptor antagonist (IL-1ra) attenuated the release of IL-6 and had a marginal effect on the corticosterone response 6 h after turpentine. These results suggest that the early and late phase of the P-A response to tissue injury are mediated by different mechanisms.
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Early HPAA activation after TPS-induced inflammation seems likely to be neurally mediated.
“The early activation seems likely to be neurally mediated, and we have previously shown that early HPAA activation is reduced by deafferentation of the medial basal hypothalamus or neonatal capsaicin treatment (13).”
From Interleukin-6 is an afferent signal to the hypothalamo-pituitary-adrenal axis during local inflammation in mice (2003) · cites this paper as [13]
Early HPAA activation is reduced by deafferentation of the medial basal hypothalamus or neonatal capsaicin treatment.
“The early activation seems likely to be neurally mediated, and we have previously shown that early HPAA activation is reduced by deafferentation of the medial basal hypothalamus or neonatal capsaicin treatment (13).”
From Interleukin-6 is an afferent signal to the hypothalamo-pituitary-adrenal axis during local inflammation in mice (2003) · cites this paper as [13]
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Self-citation
- Authors
- Turnbull, A. V., Dow, R. C., Hopkins, S. J., White, A., Fink, G., & Rothwell, N. J.
- Affiliations
- University of Manchester (GB)
- University of Edinburgh (GB)
- Corresponding author
- Turnbull, A.V.
- Venue
- Psychoneuroendocrinology
- Publisher
- Elsevier BV
- Published
- 1994
- Volume
- 19
- Issue
- 2
- Pages
- 165-178
- ISSN
- 0306-4530 (ISSN-L)
- OpenAlex
- W2135823847
- Cited by
- 49
- References
- 36
- Citations by year
- 2026: 1 · 2013: 1 · 2012: 1
- FWCI
- 2.43
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Psychoneuroendocrinology (publishedVersion)
- PubMed (publishedVersion)
- Research Explorer (The University of Manchester) (publishedVersion)
- Funders
- Wellcome Trust
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Keywords
- pituitary-adrenal axis, tissue damage, ACTH, corticosterone, turpentine, interleukin-6, interleukin-1 receptor antagonist, medial basal hypothalamus, capsaicin, deafferentation, stress response
- MeSH terms
- Acute-Phase Reaction, Adrenocorticotropic Hormone, Afferent Pathways, Animals, Animals, Newborn, Arousal, Capsaicin, Corticosterone, Hypothalamo-Hypophyseal System, Inflammation, Male, Nociceptors, Pituitary-Adrenal System, Turpentine, Interleukin-6, Rats, Sprague-Dawley, Receptors, Interleukin-1, Rats
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