Abstract
Omega-3-fatty acid DHA is a structural component of brain plasma membranes, thereby crucial for neuronal signaling; however, the brain is inefficient at synthesizing DHA. We have asked how levels of dietary n-3 fatty acids during brain growth would affect brain function and plasticity during adult life. Pregnant rats and their male offspring were fed an n-3 adequate diet or n-3 deficient diets for 15 weeks. Results showed that the n-3 deficiency increased parameters of anxiety-like behavior using open field and elevated plus maze tests in the male offspring. Behavioral changes were accompanied by a level reduction in the anxiolytic-related neuropeptide Y-1 receptor, and an increase in the anxiogenic-related glucocorticoid receptor in the cognitive related frontal cortex, hypothalamus and hippocampus. The n-3 deficiency reduced brain levels of docosahexaenoic acid (DHA) and increased the ratio n-6/n-3 assessed by gas chromatography. The n-3 deficiency reduced the levels of BDNF and signaling through the BDNF receptor TrkB, in proportion to brain DHA levels, and reduced the activation of the BDNF-related signaling molecule CREB in selected brain regions. The n-3 deficiency also disrupted the insulin signaling pathways as evidenced by changes in insulin receptor (IR) and insulin receptor substrate (IRS). DHA deficiency during brain maturation reduces plasticity and compromises brain function in adulthood. Adequate levels of dietary DHA seem crucial for building long-term neuronal resilience for optimal brain performance and aiding in the battle against neurological disorders.
Highlights
The causes of most neurological disorders are indefinite and characterized by multiple components, in which the interaction of the environment with the genome likely plays a major role
The open field (OF) and elevated plus maze (EPM) studies were performed to assess anxiety-like behavior
We found that levels of pCREB significantly decreased in the hypothalamus (t10 = 2.406, p = 0.0369) and in the hippocampus (t10 = 2.563, p = 0.0282), while no significant changes were observed in the frontal cortex (t10 = 2.022, p = 0.0707) of rats fed an n-3 deficient diet as compared to n-3 diet rats (Fig. 4C)
Summary
The causes of most neurological disorders are indefinite and characterized by multiple components, in which the interaction of the environment with the genome likely plays a major role. Dietary factors are garnering special recognition as important modifiers of brain function and plasticity, and mental heath [1]. In addition to affecting individuals at all stages of life, an alarmingly increasing number of young adults suffer from anxiety disorders [2] making it imperative to develop therapeutic strategies to moderate the incidence of mood disorders. New studies emphasize the quality of the diet as an important factor affecting the occurrence of mood disorders in a large population of adults [3]; poor knowledge on the molecular mechanisms involved has delayed the implementation of diet as a strategy for the prevention or treatment of mood disorders. DHA is delivered to the brain by maternal source via uteroplacental circulation [7], emphasizing the importance of maternal supply of n-3 fatty acids for the neurological function of the offspring. N-6 fatty acids generally compete with n-3 fatty acids for membrane occupancy such that the reciprocal relationship between n-3 and n-6 fatty acids is altered in DHA deficient conditions, imposing a risk for neuronal function [8,9]
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