H.-C. Xing

Effects of Dietary n-3 Fatty Acid Deficiency on Morris Water-Maze Performance and Amphetamine-Induced Conditioned Place Preference in Rats.

In these studies we examined whether dietary n-3 fatty acid (FA) deficiency in adult male rats was associated with effects on performance in the Morris water-maze and with the development of a conditioned place preference to low (0.5 mg/kg) and high (2.0 mg/kg) doses of amphetamine. The male rats used in these studies had been raised for two generations on n-3 deficient diets, which produced an n-6: n-3 FA ratio in brain lipids three times that of animals fed an n-3 adequate diet. Although the two groups did not differ on learning the position of the hidden platform in the Morris water-maze, the n-3 deficient rats did show deficits on a subsequent working memory version of this task, and swam longer distances to reach a visible platform. There were no differences between the groups on the development of a conditioned place preference although, during the initial conditioning cycle, the increase in activity in response to the high dose of amphetamine was apparent only in the n-3 deficient group. These findings provide preliminary support for effects of n-3 FA deficiency on working memory, but not on motivational processes as measured by response to a drug reward.

Effects of gamma-linolenic acid and docosahexaenoic acid in formulae on brain fatty acid composition in artificially reared rats.

This study evaluated the effects of dietary supple-mentation with ψ-linolenic acid (GLA, 18∶3n−6) and docosahexaenoic acid (DHA, 22∶6n−3) on the fatty acid composition of the neonatal brain in gastrostomized rat pups reared artificially from days 5–18. These pups were fed rat milk substitutes containing fats that provided 10% linoleic acid and 1% α-linolenic acid (% fatty acids) and, using a 2×3 factorial design, one of two levels of DHA (0.5 and 2.5%), and one of three levels of GLA (0.5, 1.0, and 3.0%). A seventh artificially reared groups served as a reference group and was fed 0.5% DHA and 0.5% arachidonic acid (AA, 20∶4n−6); these levels are within the range of those found in rat milk. The eighth group, the suckled control group, was reared by nursing dams fed a standard American Institute of Nutrition 93M chow. The fatty acid composition of the phosphatidylethanolamine, phosphatidyl-choline, and phosphatidylserine/phosphatidylinositol membrane fractions of the forebrain on day 18 reflected the dietary composition in that high levels of dietary DHA resulted in increases in DHA but decreases in 22∶4n−6 and 22∶5n−6 in brain. High levels of GLA increased 22∶4n−6 but, in contrast to previous findings with high levels of AA, did not decrease levels of DHA. These results suggest that dietary GLA, during development, differs from high dietary levels of AA in that it does not lead to reductions in brain DHA.

Effects of high-γ-linolenic acid canola oil compared with borage oil on reproduction, growth, and brain and behavioral development in mice

Previous research in rats and mice has suggested that γ-linolenic acid (GLA) derived from borage oil (BO: 23% GLA) may be an appropriate source for increasing levels of long-chain n−6 FA in the developing brain. Recently, transgenic technology has made available a highly enriched GLA seed oil from the canola plant (HGCO: 36% GLA). The first objective of this study was to compare the effects of diets containing equal levels of GLA (23%) from either BO or HGCO on reproduction, pup development, and pup brain FA composition in mice. The second objective was to compare the effects of the HGCO diluted to 23% GLA (GLA-23) with those of undiluted HGCO containing 36% GLA (GLA-36). The diets were fed to the dams prior to conception and throughout pregnancy and lactation, as well as to the pups after weaning. The behavioral development of the pups was measured 12 d after birth, and anxiety in the adult male offspring was assessed using the plus maze. The findings show that despite equivalent levels of GLA, GLA-23 differed from BO in that it reduced pup body weight and was associated with a slight increase in neonatal pup attrition. However, there were no significant effects on pup behavioral development or on performance in the plus maze. An increase in dietary GLA resulted in an increase in brain 20∶4n−6 and 22∶4n−6, with a corresponding decrease in 22∶6n−3. Again, despite their similar levels of GLA, these effects tended to be larger in GLA-23 than in BO. In comparison with GLA-23, GLA-36 had larger effects on growth and brain FA composition but no differences with respect to effects on reproduction and behavioral development. These findings suggest that the HGCO can be used as an alternative source of GLA.

Effects of postnatal ethanol exposure on brain growth and lipid composition in n−3 fatty acid-deficient and-adequate rats

The artificial rearing model was used to investigate the effects of short-term exposure to ethanol on growth and fatty acid composition of forebrain (FB) and cerebellum (CB) during the brain growth spurt in either n−3 fatty acid-adequate (AD) or n−3 deficient (DEF) rat pups. On postnatal day 5, offspring of female rats that had been fed AD or DEF diets from day 5 of life were assigned to three groups: members of two groups were gastrostomized and artificially fed formulas appropriate for their maternal history, and the third group (suckled control) was fostered to lactating dams of a similar dietary history. Half of the artificially reared pups in each dietary condition were fed ethanol in their formula (7% vol/vol) in one-quarter of their daily feedings, while the others received maltose-dextrin substituted isocalorically for ethanol. Blood alcohol concentrations did not differ betwen the dietary groups. FB weight on postnatal day 9 was lower in ethanol-exposed offspring in both dietary conditions. Brain fatty acid composition reflected dietary history in that, compared with AD pups, DEF pups had lower percentages of docosahexaenoic acid, higher percentages of 22∶5n−6, and a higher n−6/n−3 fatty acid ratio. However, the effects of ethanol exposure were inconsistent, lowering the n−6/n−3 ratio in the phosphatidylethanolamine (PF) fraction in FB but not in CB, while increasing this ratio in the phosphatidylcholine (PC) fraction in FB of the DEF pups only. Thus, while ethanol had some effects on lipid composition, there was no difference between the dietary groups in their vulnerability to the effects of early short-term ethanol exposure on brain growth.