Effects of stress on susceptibility and severity of inflammation in adjuvant-induced arthritis

We have utilized the open field and learned helplessness (LH) models of psychological stress to determine whether a differential response to stress can affect the severity of adjuvant-induced arthritis (AA) within a single rat strain. In response to open field stress, the corticosterone response of...

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Bibliographic Details
Published in:Annals of the New York Academy of Sciences 1999-06, Vol.876 (1), p.276-286
Main Authors: Chover-Gonzalez, A J, Harbuz, M S, Tejedor-Real, P, Gibert-Rahola, J, Larsen, P J, Jessop, D S
Format: Article
Language:English
Subjects:
Animals
Arthritis, Experimental - blood
Arthritis, Experimental - etiology
Arthritis, Experimental - pathology
Arthritis, Experimental - physiopathology
Avoidance Learning - physiology
Corticosterone - blood
Disease Susceptibility
Electroshock
Foot
Helplessness, Learned
Male
Rats
Rats, Wistar
Reference Values
Stress, Physiological - physiopathology
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Summary:We have utilized the open field and learned helplessness (LH) models of psychological stress to determine whether a differential response to stress can affect the severity of adjuvant-induced arthritis (AA) within a single rat strain. In response to open field stress, the corticosterone response of the low emotivity rats was significantly lower than that of the high emotivity rats. In spite of the differential corticosterone response to stress, no significant difference was found in paw volumes between the AA high and low emotivity groups. In another study, rats were subjected to a learned LH paradigm and separated into two groups based on failed (LH+) or successful (LH-) avoidance. Plasma corticosterone levels in response to avoidable foot shock in the LH- rats were significantly greater than in the LH+ group. Following injection with adjuvant, paw inflammation occurred earlier and was more severe in the LH- rats compared to the LH+ group. These data show that rats with a greater tendency to avoid foot shock have more severe inflammation, despite having a greater corticosterone response to stress. We conclude that an increased corticosterone response to stress does not affect susceptibility to or severity of inflammation in AA. Indeed, in the LH model a more robust response to stress is associated with increased inflammation and earlier onset of the disease.
ISSN:0077-8923
1749-6632
DOI:10.1111/j.1749-6632.1999.tb07650.x