Figure 2.

Top: exposure to stress (arrow) leads to a temporary rise in the circulating corticosterone concentration. After approximately two hours, levels are back to the prestress level. Bottom: the consensus view is that exposure to stress reduces NMDA-type LTP in the CA1 area (solid black bar), in a slow gene-mediated fashion. At the same time, LTD is facilitated (striped black bar). Recent studies (greyish bars) have elaborated this view. At the initial phase of the stress response (i.e., as long as corticosteroid levels are really elevated) LTP is increased (solid grey bar); this is most likely due to a nongenomic effect of corticosterone, in concert with the effects of CRH and noradrenaline. At a later time scale (when corticosteroid levels have normalized again), VDCC- (as opposed to NMDA-) type of LTP is increased (stippled grey bar). While LTP in the CA1 area is reduced by stress, LTP in the dentate gyrus (DG) can be enhanced (vertical striped grey bar). Chronic stress suppresses LTP, under basal conditions as well as some time after exposure to elevated corticosteroid levels (horizontal striped grey bar). The black arrow indicates the direction of change in LTP as agreed for gene-mediated effects of high doses of corticosterone on NMDA-type LTP in the CA1 area. The grey arrow indicates the direction for changes regarding the dentate gyrus, VDCC-type of LTP, and rapid nongenomic effects.