The brain is the organ with the second greatest concentration of lipids; they are directly involved in the functioning of membranes. Brain development is genetically programmed; it is therefore necessary to ensure that nerve cells receive an adequate supply of lipids during their differentiation and multiplication. Indeed the effects of polyunsaturated fatty acid (PUFA) deficiency have been extensively studied; prolonged deficiency leads to death in animals. Linoleic acid (LA) is now universally recognized to be an essential nutrient. On the other hand, alpha-linolenic acid (ALNA) was considered non-essential until recently, and its role needs further studies.In our experiments, feeding animals with oils that have a low alpha-linolenic content results in all brain cells and organelles and various organs in reduced amounts of 22:6(n-3), compensated by an increase in 22:5(n-6). The speed of recuperation from these anomalies is extremely slow for brain cells, organelles and microvessels, in contrast with other organs. A decrease in alpha-linolenic series acids in the membranes results in a 40% reduction in the Na-K-ATPase of nerve terminals and a 20% reduction in 5′-nucleotidase. Some other enzymatic activities are not affected, although membrane fluidity is altered. A diet low in ALNA induces alterations in the electroretinogram which disappear with age: motor function and activity are little affected but learning behaviour is markedly altered. The presence of ALNA in the diet confers a greater resistance to certain neurotoxic agents, i.e. triethyl-lead.We have shown that during the period of cerebral development, there is a linear relationship between brain content of (n-3) acids and the (n-3) content of the diet up to the point where alpha-linolenic levels reach 200 mg for 100 g food intake. Beyond that level there is a plateau. For the other organs, such as the liver, the relationship is also linear up to 200 mg100 g, but then there is merely an abrupt change in slope and not a plateau. By varying the dietary 18:2(n-6) content, it was noted that 20:4(n-6) optimum values were obtained at 150 mg100 g for all nerve structures, at 300 mg for testicle and muscle, 800 mg for the kidney, and 1200 mg for the liver, lung and heart. A deficiency in ALNA or an excess of LA has the same main effect: an increase in 22:5(n-6) levels.Taking into account that the relative metabolisms of man and the rat, their rates of development, the difference between their brain/body weight ratios, and the similar fatty acid (FA) composition of their nerve membranes, it is possible to affirm that results obtained in the rat are necessarily, and at the very least, valid for man. For the brain and the other organs, the requirement in ALNA acid is 200 mg100 g food intake (0.4% of calories), provided that LA requirements of 1200 mg100 g food intake (2.4% of calories) are met.During pre and postnatal development, delta-6 desaturase in brain decreases dramatically (12-fold) up to postnatal day 21 and remains nearly constant thereafter. In liver, the activity increases approximately 9-fold between day 3 before birth and day 7 after birth. Then, it decreases slightly up to weaning and is approximately constant up to 4 months. From the on delta-6-desaturase decreases with age (40% between 4 and 17 months). The question remains whether the residual delta-6 desaturase activity after day 21 is sufficient to support the turnover of brain membranes. If it is not, the very-long-chain FA would have to be synthesized by the liver. As liver synthesis decreases during aging this source may be insufficient. It should be noted that cultured nerve cells differentiate, multiply, take up and release neurotransmitters only if the medium contains 20:4(n-6) and 22:6(n-3), but not if it contains 18:2(n-6) and 18:3(n-3). Thus, the FA that are essential for the brain could be those with very long chains. They are probably synthesized in the liver from ALNA and LA. They can also be furnished directly by the diet.However a dietary excess of fish oil can prove to be toxic due to perturbation of the composition of cerebral membranes. Pharmacological doses of fish oil do not alter FA composition of liver and brain, and do not change protection against peroxidation. In contrast, increasing dietary fish oil in rat had the following effects on brain lipids: 20:4(n-6) regularly decreased; cervonic acid was increased by 30% at high fish oil concentration.PUFA in membranes are protected against peroxidation, mainly by vitamin E. In peripheral nervous system during development and aging a highly significant correlation between vitamin E and (n-6) PUFA was observed but not between (n-3) PUFA and vitamin E.

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{{Explor lien
   |wiki=    Wicri/Musique
   |area=    MozartV1
   |flux=    France
   |étape=   Analysis
   |type=    RBID
   |clé=     ISTEX:CE2906CF73E1D14F96EADB153610406916D6588D
   |texte=   Function of dietary polyunsaturated fatty acids in the nervous system
}}