Excessive or pathological levels of anxiety induce maladaptive responses. Indeed, anxiety has a key biological-adaptive role, which is highly conserved during evolution. Anxiety is an adaptive reaction induced when an animal is confronted with potential demands and dangers. These alterations increase anxiety, and impair both memory and spatial learning. Ĭhronic stress and corticosterone treatment affect the dendritic morphology of limbic areas of the rat brain, such as the hippocampus, amygdaloid complex, and prefrontal cortex. Chronic glucocorticoid treatment induces dendritic atrophy in the hippocampus and medial prefrontal cortex, while acute corticosterone treatment induces dendritic hypertrophy in the basolateral amygdaloid nucleus and enhances anxiety. The hippocampus, amygdala and medial prefrontal cortex have high concentrations of GRs. Corticosterone is bound to glucocorticoid receptors (GRs) in peripheral tissues and the brain. Stressors increase the release of corticotrophin releasing factor (CRF) from the hypothamus, inducing adrenocorticotropic hormone release from the anterior pituitary, which in turn stimulates the secretion of corticosterone from the adrenal cortex. Stress responses are mainly mediated by the activation of the hypothalamic-pituitary-adrenal (HPA) axis, leading to secretion of glucocorticoids from the adrenal gland glucocorticoids are bound to glucocorticoid receptors in peripheral tissues and the brain to regulate stress responses. Stress is a complex biological reaction common to all living organisms that allows them to adapt to environmental pressure (i.e., stressors). Thus, our results demonstrate that ω-3 supplementation had two beneficial effects on the stressed rats, a strong anti-stress effect and improved learning. These alterations were prevented by ω-3 supplementation. Restraint stress impaired learning and increased both corticosterone levels and the number of entries into the open-arm (elevated plus-maze). As well, plasma corticosterone levels and anxiety were evaluated as stress markers, respectively by ELISA and the plus-maze test. Afterwards, learning was analyzed by avoidance conditioning. 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. 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). The aim of this study was to evaluate the effects of ω-3 supplementation on learning and major biological and behavioral stress markers. Supplementation with ω-3 fatty acids improves memory and learning in rats. Both alterations have been correlated with memory impairment and increased anxiety. Chronic stress leads to secretion of the adrenal steroid hormone corticosterone, inducing hippocampal atrophy and dendritic hypertrophy in the rat amygdala.