Coping with the Forced Swim Stressor: Towards Understanding an Adaptive Mechanism

Figure 5

Hypothesis: processing of the forced swim stressor. ① The stressor is perceived and appraised and the appropriate coping style is selected depending on flexibility of amygdala-hippocampus-striatal connectivity, which is controlled by CORT via limbic MR. ② This action of CORT mediated by MR modulates the hippocampal excitatory outflow through enhanced glutamate transmission driving the spontaneous activity of the VTA-A9 neurons and active coping. ③ When time elapses energy is allocated to more executive functions governed by mesocortical and prefrontal circuitry attenuating mesoaccumbens dopamine activity causing a switch from active to passive coping with the inescapable forced swim stressor. ④ The coping response is stored in memory for future use by a mechanism activated by stress-induced levels of CORT acting through the GR in the hippocampal dentate gyrus. ⑤ The information processing during the forced swim is affected by stress history as can be deducted from altered genomic expression in the hippocampus. This hypothesis is based on the following references: [14–19, 28, 30, 31, 36, 50, 51, 58, 64, 82, 84, 94, 102, 110–114]. For more information we refer to the main text of this paper. CORT is corticosterone; MR is mineralocorticoid receptors; GR is glucocorticoid receptors; VTA is ventral tegmental area, A9 dopaminergic neurons.