Advanced age is associated with reduced brain levels of long-chain polyunsaturated fatty acids, arachidonic acid (AA) and docosahexaenoic acid (DHA). Memory impairment is also a common phenomenon in this age. Two-year-old, essential fatty acid-sufficient rats were fed with fish oil (11% DHA) for 1 month, and fatty acid as well as molecular composition of the major phospholipids, phosphatidylcholine and phosphatidylethanolamine (PE), was compared with that of 2-month-old rats on the same diet. DHA but not AA was significantly reduced in brains of old rats but was restored to the level of young rats when they received rat chow fortified with fish oil. This effect was pronounced with diacyl 18:0͞22:6 PE species, whereas levels of 18:1͞22:6 and 16:0͞22:6 remained unchanged in all of the three PE subclasses. Fish oil reduced the AA in the old rat brains, diacyl and alkenylacyl 18:0͞20:4 PE being most affected. Phosphatidylcholines gave less pronounced response. Six genes were up-regulated, whereas no significant changes were observed in brains of old rats receiving fish oil for 1 month. None of them except synuclein in young rat brains could be related to mental functions. Old rats on the fish-oil diet did not perform better in Morris water maze test than the control ones. A 10% increase in levels of diacyl 18:0͞22:6 PE in young rat brains resulted in a significant improvement of learning capacity. The results are interpreted in terms of the roles of different phospholipid molecular species in cognitive functions coupled with differential responsiveness of the genetic machinery of neurons to n-3 polyunsaturated fatty acids.B rain is one of the organs rich in phospholipids, which provide the building blocks for different membrane structures. These phospholipids are rather rich in long-chain polyunsaturated fatty acids, particularly in docosahexaenoic acid (DHA) and arachidonic acid (AA). DHA content of brain phospholipids seems to be precisely controlled. It is determined during pregnancy and early postnatal life (1, 2). There is a consensus that after this time it is almost impossible to alter brain fatty acid composition of adult, essential fatty acid-sufficient rats. On the other hand, any imbalance in polar head group or fatty-acid composition of structural lipids might have consequences on mental performance. Loss in DHA in brains of persons with Alzheimer's disease is accompanied with loss of memory and learning (3). In aged persons, impairment of memory also often takes place, and this is accompanied with loss of DHA in their brains (4-6). It has been shown that chronic administration of DHA to essential fatty acid-deficient young rats restores DHA levels in brain and improves memory (7). Similarly, DHA administration to ischemic rats had beneficial effect on spatial cognitive deficit (8). Moriguchi et al. (9) showed also that full recovery of brain DHA in essential fatty acid-deficient rats was obtained after 8 weeks on a DHA-containing diet. Hashimoto et al. (10) demonstrated that DHA provided protection fr...

The hypothalamo-pituitary-adrenal (HPA) axis plays a central role both in the regulation of the stress response, and in the control of feeding behaviour. Sensitivity of the HPA axis to respond to stress varies both during ontogeny and between individuals, and can be altered by neonatal events. The aim of our experiments was to determine whether early events that affect the HPA axis could also induce persistent modifications in food intake (quantitatively and qualitatively), as well as alterations of anxiety-related behaviour. Twenty-four-hour maternal deprivation was introduced at two different periods of HPA maturation, on day 5 (DEP5) or day 14 (DEP14) after birth. Sequential measurements of plasma levels of adrenocorticotropin hormone (ACTH) and corticosterone showed that this deprivation altered the HPA axis of adults; the response to restraint stress was prolonged in DEP5 and a higher ACTH peak appeared in DEP14. The neonatal stress also produced long-lasting modifications of rat behaviour, as DEP14 adults became more anxious. Standard food intake decreased in both groups of deprived rats. Diet preferences also changed, as carbohydrate intake decreased in DEP5 rats. Corticosteroid receptor binding did not vary in the hippocampus of the deprived rats. The modifications of the stress response and the behaviour parameters could be due to the alteration of corticosteroid receptors in the hypothalamic paraventricular nucleus and/or corticotropin-releasing hormone or vasopressin function, but these parameters have yet to be determined. This early stress paradigm altering feeding behaviour could become an interesting model for research into human eating disorders.