Abstract
Chronic stress leads to secretion of the adrenal steroid hormone corticosterone, inducing hippocampal atrophy and dendritic hypertrophy in the rat amygdala. Both alterations have been correlated with memory impairment and increased anxiety. Supplementation with ω-3 fatty acids improves memory and learning in rats. The aim of this study was to evaluate the effects of ω-3 supplementation on learning and major biological and behavioral stress markers. Male Sprague–Dawley rats were randomly assigned to three experimental groups: 1) Control, 2) Vehicle, animals supplemented with water, and 3) ω-3, rats supplemented with ω-3 (100 mg of DHA+25 mg of EPA). Each experimental group was divided into two subgroups: one of which was not subjected to stress while the other was subjected to a restraint stress paradigm. Afterwards, learning was analyzed by avoidance conditioning. As well, plasma corticosterone levels and anxiety were evaluated as stress markers, respectively by ELISA and the plus-maze test. Restraint stress impaired learning and increased both corticosterone levels and the number of entries into the open-arm (elevated plus-maze). These alterations were prevented by ω-3 supplementation. Thus, our results demonstrate that ω-3 supplementation had two beneficial effects on the stressed rats, a strong anti-stress effect and improved learning.
Highlights
Stress is a complex biological reaction common to all living organisms that allows them to adapt to environmental pressure [1,2]
There was a main effect of diet and interaction on body weight gain, where the post-hoc test showed that rats subjected to restraint stress from both control and ω-3 diet groups had significantly decreased body weight gain compared to the respective unstressed controls (F(1,48) = 1559, p < 0.0001)
Body weight gain of rats from the vehicle group subjected to restraint stress was not affected compared to unstressed rats from the vehicle group (Figure 2A)
Summary
Stress is a complex biological reaction common to all living organisms that allows them to adapt to environmental pressure (i.e., stressors) [1,2]. Chronic stress and corticosterone treatment affect the dendritic morphology of limbic areas of the rat brain, such as the hippocampus, amygdaloid complex, and prefrontal cortex [17,18,19]. These alterations increase anxiety, and impair both memory and spatial learning [20,21,22]. Chronic stress or psychosocial stress produces hippocampal volume atrophy [24] and functional changes in the prefrontal cortex [25]
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