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.