Long-term effects of perinatal essential fatty acid deficiency on anxiety-related behavior in mice.

Abstract

Dietary essential fatty acids have been shown to regulate behavioral and cognitive functions in rodents. However, the long-term effect on behavior, besides memory and learning, of essential fatty acid deficiency (EFAD), i.e., lack of n-3 and n-6 fatty acids, during the perinatal period has not been investigated. Therefore, pregnant C57Bl/6 mice were given either an EFAD or an isoenergetic control diet from gestational day 16 and throughout lactation. The female offspring were given standard chow from 3 weeks of age, and at 12 to 14 weeks of age, open-field, object recognition, light-dark transition, elevated plus maze, and social interaction tests were performed. The brain glycerophospholipid fatty acid composition was investigated in 3-week-old and adult offspring by gas chromatography. The differences observed in behavior were indicative of lower anxiety in the EFAD mice compared to controls illustrated by more time spent in the open arms of the elevated plus maze (+ 41%, p < .05) and in the light compartment in the light-dark transition test (+ 63%, p < .05). The proportion of total n-3 fatty acids, especially 22:6n-3 in the brain, was lower with a compensatory increase in the proportion of total n-6 fatty acids, foremost 22:5n-6, in the EFAD mice compared to controls at 3 weeks of age. In the adult brains the fatty acid composition was normalized. In conclusion, our data show that EFAD during the perinatal period results in short-term alterations of fatty acid composition in brain and decreased anxiety in adult life.

Dietary long chain n-3 polyunsaturated fatty acids prevent impaired social behaviour and normalize brain dopamine levels in food allergic mice

“…Supplementation with N-3 LCPUFA enhanced n-3 DHA content in the brain, mainly at the expense of n-6 AA and DTA. LCPUFA, in particular AA and DHA (Palsdottir et al, 2012), are incorporated in the neuronal cell membrane to maintain normal brain function (Schuchardt et al, 2010;Bourre et al, 1991;Uauy and Dangour, 2006). Brain fatty acid content is dependent on nutritional intake and it was shown that suboptimal n-3 LCPUFA intake during gestation and postnatal development caused neurodevelopmental deficits in preclinical (Chen and Su, 2013;Bhatia et al, 2011) and clinical studies (Birch et al, 2000;Willatts et al, 1998;Drover et al, 2011).…”

Cognitive enhancement by omega-3 fatty acids from child-hood to old age: Findings from animal and clinical studies

“…Brain lipid profile (rat). Brain lipid profile, adapted from Palsdottir et al (2012). C18:0: stearic acid; C18:2, n-6: linoleic-acid (LA); C20:3, n-6: Dihomo-gamma-linolenic acid (DGLA); C20:4, n-6: arachidonic acid (AA); C22:5, n-6: Docosapentaenoic acid (DPA); C18:3, n-3: Alpha-linolenic acid (ALA); C20:5, n3: Eicosapentaenoic acid (EPA); C22:5, n-3: Docosapentaenoic acid (DPA); C22:6, n-3: Docosahexaenoic acid (DHA).…”

Modulation of prenatal stress via docosahexaenoic acid supplementation: implications for child mental health

“…These studies are summarized in Table 1 for experimental rodent models and in Table 2 for experimental and observational studies in humans. In experimental rodent models, deficient levels of DHA during pregnancy resulted in deficits in learning, such as habituation to novelty and latency to reach learning criteria 50 ; prolonged corticosterone response to restraint stress and longer periods of immobility during the Porsolt forced swim test 51 ; and less exploration of environmental stimuli in the offspring, 52 as determined via tests designed to assess constructs similar to distress disorders in humans. Takeuchi et al 41 demonstrated that pups of DHA-deficient dams spent less time in the open arms of a plus maze (indicative of higher stress levels) than the offspring of normally fed animals.…”