Abstract
Depressive symptoms are often accompanied by cognitive impairments and recurrent depressive episodes are discussed as a potential risk for dementia. Especially, stressful life events are considered a potent risk factor for depression. Here, we induced recurrent stress-induced depressive episodes over the life span of rats, followed by cognitive assessment in the symptom-free period. Rats exposed to stress-induced depressive episodes learned faster than control rats. A high degree of stress-induced depressive-like behavior early in the paradigm was a predictor of improved cognitive performance, suggesting induction of resilience. Subsequently, exposure to lorazepam prior to stress-induced depressive episodes and cognitive testing in a nonaversive environment prevented the positive effect. This indicates a beneficial effect of the stress-associated situation, with the existence of individual coping abilities. Altogether, stress may in some have a beneficial effect, yet for those individuals unable to tackle these aversive events, consecutive unpleasant episodes may lead to worse cognitive performance later in life.
Highlights
A history of recurrent depression episodes has been suggested to constitute a risk factor for dementia, such that vulnerability toward dementia has been correlated to the frequency of the depressive episodes, with recurrent episodes increasing the risk[1]
The aim of this study was to investigate the impact of recurrent stress-induced depression on later cognitive performance
The level of stress experience and depressive-like behavior measured during the first learned helplessness (LH) episode served as a predictor of the later performance in the cognitive tasks
Summary
A history of recurrent depression episodes has been suggested to constitute a risk factor for dementia, such that vulnerability toward dementia has been correlated to the frequency of the depressive episodes, with recurrent episodes increasing the risk[1]. The experience of being unable to avoid or handle stressful life events is considered a potent risk factor for depression[3,4,5,6,7], and is implemented in the learned helplessness (LH) paradigm that induces a transient, depressive phenotype in rodents[8]. The experience of unescapable stress induces helplessness and subsequent anhedonia-like behavior in the animal, whereas on a neurobiological-level serotonergic dysregulation, decrease in brain-derived neurotrophic factor (BDNF) levels and hippocampal deficits become evident[9,10,11,12].
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