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Interleukin 1 beta enhances conditioned fear memory in rats: possible involvement of glucocorticoids
Author(s) -
Song Cai,
Phillips Anthony G.,
Leonard Brian
Publication year - 2003
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.2003.02886.x
Subject(s) - corticosterone , mifepristone , glucocorticoid , endocrinology , medicine , antagonist , cytokine , facilitation , receptor antagonist , interleukin , psychology , prostaglandin e2 , receptor , neuroscience , biology , hormone , pregnancy , genetics
Central administration of 15 ng interleukin (IL)‐1β in the rat significantly enhanced conditioned fear memory assessed by a passive avoidance task, when retested at 24 and 48 h post‐training. Pain threshold was unaffected by 15 ng IL‐1β administration. IL‐1β treatment also increased serum corticosterone. This increase in serum corticosterone was further enhanced in rats given both IL‐1β and footshock. Furthermore, the glucocorticoid receptor antagonist mifepristone blocked IL‐1β‐induced elevation in corticosterone and also attenuated the enhanced conditioned fear memory. Central administration of IL‐1β significantly increased prostaglandin E 2 and decreased the anti‐inflammatory cytokine IL‐10 release from whole blood cultures; therefore this treatment appears to be effective in inducing an inflammatory response in both the periphery and the brain. The present study confirms that IL‐1β can enhance conditioned fear memory, an effect which is correlated with changes in glucocorticoid function. This facilitation of defensive behaviour could reflect adaptive responses which may enhance survival during sickness.