Cytokine involvement in stress may depend on corticotrophin releasing factor to sensitize @entity1068 withdrawal XXXX .

@entity1246 @entity657 @entity1505 @entity2819 @entity148 @entity3318 @entity35 @entity72945 @entity37257 @entity1068
Stress has been shown to facilitate @entity1068 withdrawal-induced @entity148 . Defining neurobiological mechanisms through which stress has such actions is important given the associated risk of relapse. While @entity3318 has long been implicated in the action of stress, current results show that stress elevates the cytokine @entity1505 in the @entity35 brain and thereby implicates cytokines in stress effects. In support of this view, prior @entity1505 microinjection into the central amygdala (CeA) of @entity35 facilitated @entity1068 withdrawal-induced @entity148 -a response that could not be attributed to an increase in plasma @entity2819 . To test for a possible interaction between cytokines and @entity3318 , a CRF1-receptor antagonist ( @entity72945 ) administered prior to the repeated administration of @entity1505 or @entity657 / @entity657 reduced the magnitude of the withdrawal-induced @entity148 . This finding provided evidence for cytokine action being dependent upon @entity3318 . Additionally, the sensitizing effect of stress on withdrawal-induced @entity148 was reduced by treating the repeated stress exposure prior to @entity1068 with the MEK inhibitor @entity37257 . Consistent with cytokines having a neuromediator function distinct from a neuroimmune action, @entity1505 increased firing rate and @entity1246 release from CeA neurons. Thus, an interaction of glial and neuronal function is proposed to contribute to the interaction of stress and chronic @entity1068 . Interrupting this potential glial-neuronal interaction could provide a novel means by which to alter the development of emotional states induced by stress that predict relapse in the alcoholic.
