Developmental binge exposure to ethanol and artificial rearing do not affect the social transfer of diet preference.

BACKGROUND: A previous study reported no effect of binge exposure to ethanol during the brain growth spurt on the social acquisition of enhanced diet preference in male rats. The objective of this study was to replicate this finding by using the artificial rearing technique and to investigate whether delay-dependent mnemonic deficits previously observed in the water maze would extend to social memory of diet preference. We also addressed whether this naturalistic behavior was dependent on the presentation of diet odor in the context of a rat-produced component in ethanol-exposed rats, as it is in normal controls. METHODS: Male rat pups were reared artificially from postnatal days 5 to 18, during which (postnatal days 6-9) they were fed either 6.5 g/kg/day of ethanol in a binge model or an isocaloric maltose-dextrin solution (gastrostomy controls). A third suckled control group was reared normally. These test rats were allowed to interact with conspecifics that had previously consumed a distinctive diet, X. Subsequently, the experimental rats were provided a choice between two novel diets, one of which was X, after delays of 0 hr (experiment 1), 24 hr, and 4 weeks (experiment 2). In experiment 3, the rats were again given the two-choice preference test, but after exposure to the diet odor alone. RESULTS: All groups demonstrated a significant preference for the socially cued diet in experiments 1 and 2, and the strength of this inclination remained consistent across the 0-hr, 24-hr, and 4-week retention intervals. Moreover, all groups demonstrated sensitivity to the social context of this task, as shown by a lesser preference for the diet exposed alone in experiment 3. CONCLUSIONS: Intact performance on the ethologically meaningful diet-preference test supports specificity in the cognitive/behavioral effects of developmental exposure to ethanol. Interestingly, early isolation, as experienced in the artificial-rearing procedure, also did not impair performance on this social task.

Exposure to ethanol and nicotine during the brain growth spurt: spatial DMP performance in male rats.

Male Long-Evans rats were reared artificially and, using a 2x2 design, were exposed from postnatal days (PD) 6-9 to ethanol (ET: 6.5 g kg(-1) day(-1) "binge" exposure) and/or nicotine bitartrate (NIC: 6 mg kg(-1) day(-1) continuous exposure) via gastrostomy tubes. Controls were administered maltose-dextrin in amounts isocaloric to ET and/or sodium bitartrate. A fifth suckled-control group was reared normally. NIC accelerated eye opening on PD 14; whereas ET delayed eye opening and hindlimb support on PD 16. Beginning in postnatal week 7, rats were tested on a spatial delayed matching-to-place (DMP) version of the Morris water maze, which entailed a series of problems, each consisting of search and recall trials, that required the rats to use extra-maze cues to locate a hidden escape platform. In Phase 1 of testing, the ET-exposed groups were impaired in the recall trials, but there was no effect of NIC. A longer encoding time (45 vs. 10 s) improved performance across all groups. In contrast, acute administration of NIC (0.1 mg/kg ip) immediately prior to testing in Phase 2 failed to improve performance in any group. In conclusion, these results confirm previous findings of impaired spatial DMP-task performance in ET-exposed rats and further suggest that these memory deficits are amenable to amelioration.

Intergenerational effects of complete maternal deprivation and replacement stimulation on maternal behavior and emotionality in female rats.

The present study investigated the effects of early rearing experiences on the development of maternal behavior in Sprague-Dawley female rats. Pups from individual litters were assigned to four different groups on Day 3 of life. From days 4 to 20 of life, these were reared artificially, without mother and receiving minimal "licking-like" tactile stimulation (AR-MIN), or maximal stimulation (AR-MAX) or were reared with their mothers (MR-CONTROL and MR-SHAM). At 70-100 days all AR and MR animals were mated and then observed with their own offspring, culled to eight pups. After maternal testing open-field tests were conducted. The female offspring in these litters (all raised by their MR and AR mothers) were reared to adulthood and then observed interacting with their offspring. Results show that in adulthood AR mothers engaged in significantly fewer pup-retrievals and less pup-licking (genital and body), and crouching, but significantly more non-maternal tail-chasing, digging, and hanging/climbing. As well, they were more active in the open field. Comparisons between the two AR groups and the MR groups, showed that most of the differences were between the AR-MIN and MR groups, with the AR-MAX animals showing levels of behavior between the two, and differing from neither. Analyses of covariance indicated that early experience and adult emotional behavior both influence adult maternal behavior, but their effects are independent of one another. A cross-generational effect of artificial rearing was also found. Daughters of AR and MR mothers that were observed after the birth of their own litters in adulthood showed a pattern of behavior that mimicked the pattern shown by their mothers. These results are discussed in terms of the variety of possible behavioral, endocrine, and neurochemical mechanisms that mediate the effects of early experiences on adult maternal behavior.

Varying physiological response to arm-crank exercise in specific spinal injuries.

The purpose of this arm-crank ergometry (ACE) study was to provide a greater understanding of the influence to which specific cervical and thoracic spinal cord injuries contribute to reduction in optimal cardio-respiratory and metabolic function. Twenty five male volunteers aged 20 to 47 years participated. Twenty disabled wheelchair-confined spinal cord injured (SCI) subjects were equally divided into four 'site-specific' groups based on the lesion being within either high- or low- cervical or thoracic anatomical regions. Five physically non-disabled controls (As) were included. Measured variables tended to decrease progressively from As to high-level quadriplegics. Analysis revealed a high variance in maximum cardio-respiratory performance levels between groups (P < 0.001). These findings confirm that limitation to upper body physical capabilities in the SCI during high-intensity ACE is dependent on specific lesion site. Considerable variability in performance levels were measured in those suffering lesions within closely approximating anatomical regions. Results also suggest a greater importance in the location of cervical rather than thoracic injuries in contributing towards higher relative losses in maximal cardio-respiratory and metabolic potential. Alterations in body composition and varying severity of muscle paralysis likely also play a contributing role in reducing optimal metabolic function in SCI individuals. The importance for stringent classification techniques of spinal cord lesion site in predicting upper body physical exercise potential in the SCI has therefore been highlighted in this study.

Early postnatal ethanol exposure has long-term effects on the performance of male rats in a delayed matching-to-place task in the Morris water maze.

BACKGROUND: There is concern that, in the absence of full-blown fetal alcohol syndrome, binge drinking during pregnancy might produce long-term cognitive deficits in offspring. Spatial working memory might be particularly vulnerable in this regard. This is the first study to address this issue in an animal model of binge exposure during the brain growth spurt using a delayed matching-to-place (DMTP) task in the Morris water maze. METHODS: Infant male rats were gastrostomized and reared artificially from postnatal days (PD) 5 to 18. From PD 6 to 9 they were fed either 6.5 g x kg(-1) x d (-1) ethanol (EtOH) in a binge exposure model (BAC 302 mg/dl) or an isocaloric maltose-dextrin solution (MD). The study included a third suckled control group (SC) that was reared normally. The rats were tested on a series of problems in the DMTP task, first as juveniles (PD 35) and then twice again as adults. Each problem included an initial search trial and a subsequent test trial. The first two phases of testing used delays of either 0 sec or 60 sec between these two trials. The third phase increased this delay to 60 sec and 2 hr. In addition, the rats were tested on a cued task in the water maze. RESULTS: EtOH rats were impaired relative to controls in their ability to relocate the hidden platform on the second trial, which followed the search trial. In Phases 1 and 2, there was no differential effect of ethanol on performance across the 0-sec and 60-sec delay conditions. However, EtOH rats were more affected by the longer 2-hr delay in Phase 3. There were no group differences on the search trial, in swimming speed, or cued-task performance. CONCLUSIONS: These findings establish that binge exposure to ethanol during the brain growth spurt results in a long-lasting impairment on the DMTP performance of rats in the water maze.

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 between 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 (PE) 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.

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 supplementation with gamma-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% alpha-linolenic acid (% fatty acids) and, using a 2x3 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 group 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, phosphatidylcholine, 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.

Water maze performance is unaffected in artificially reared rats fed diets supplemented with arachidonic acid and docosahexaenoic acid.

Four groups of male Long-Evans rats were reared artificially from postnatal d 5 to 18 by being fed through a gastrostomy tube with rat milk substitutes containing oils providing 10% linoleic acid and 1% alpha-linolenic acid (g/100 g fat); with the use of a 2 x 2 design, they were fed one of two levels of arachidonic acid (AA) and docosahexaenoic acid (DHA) (0.0 and 2.5 g/100 g of fatty acids). A fifth artificially reared group was fed a diet high in saturated fat, and a sixth group was reared by dams fed a standard AIN-93M diet. The pups were weaned onto modified AIN-93G diets, with a fat composition similar to that fed during the artificial rearing period. Behavioral testing was conducted between 6 and 9 wk of age; brain lipid composition was then assessed. Relative to the unsupplemented group (0.0 g/100 g AA and DHA), dietary supplementation resulted in a wide range of AA (84-103%) and particularly DHA (86-119%) levels in forebrain membrane phospholipids. AA supplementation increased AA levels and decreased DHA levels, and DHA supplementation increased DHA levels and decreased AA levels, with the magnitude of these effects dependent on the level of the other fatty acid. DHA levels were very low in the saturated fat group. The groups did not differ on the place or cued version of the Morris water-maze, but on a test of working memory, the saturated fat group was impaired relative to the suckled control group. Further correlational analyses in the artificially reared animals did not support a relationship between the wide range of DHA and AA levels in the forebrain and working-memory performance.

Long-chain polyunsaturated fatty acid levels in formulae influence deposition of docosahexaenoic acid and arachidonic acid in brain and red blood cells of artificially reared neonatal rats.

We studied the effects of dietary long-chain polyunsaturated fatty acids (PUFA) on the fatty acid composition of the brain and red blood cells in gastrostomized rat pups reared artificially from postnatal Days 5-18. These pups were fed rat milk substitutes in which the fat comprised 10% linoleic acid and 1% alpha-linolenic acid and, using a 3 x 3 factorial design, one of three levels of both arachidonic acid (AA) and docosahexaenoic acid (DHA) supplied as single cell microbial oils (0.0, 0.4 and 2.4% fatty acids). A tenth group was reared by nursing dams. The fatty acid composition of the phosphatidylethanolamine (PE) and phosphatidylserine/phosphatidylinositol (PS/PI) phospholipids in the brain and red blood cells on Day 18 reflected the dietary composition in that pups receiving long-chain supplementation of each had higher levels of the supplemented PUFA, but lower levels of the other, relative to unsupplemented groups. In contrast to these results, there were few changes in the brain in phosphatidylcholine (PC) phospholipids whereas, in the red blood cells, changes in PC were similar to those in PE and PS/PI. Regression analyses showed that DHA levels in the brain correlated more closely with those of the red blood cells than did AA levels. The results of this study indicate that, although supplementation of formula with AA or DHA during the period of rapid brain development in rats increases deposition of the long-chain PUFA in the developing tissues, each also affects the levels of the other.

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.

The incidence of chronic headache in children with shunted hydrocephalus.

Report of chronic headache amongst children with shunted hydrocephalus is frequent, and often leads to investigation for raised intra-cranial pressure and shunt malfunction, and much debate has appeared in the literature concerning possible cause. However headache is a common neurological symptom amongst children, and studies of prevalence indicate incidence of frequent non-migrainous headache to be 6.8%, and migrainous headache 4% in the general child population. A relationship between stress and anxiety and headache is recognised, and the hydrocephalic child has many reasons above those of his/her peers to be subject to stress. It is also hypothesised that this group may be more vulnerable than peers to developing a migraine-like condition in the face of adequate shunt function. The clinician dealing with complaint of chronic headache in a hydrocephalic child must therefore be wary of over-investigation in a child with a working shunt, or missing possible shunt malfunction when the only symptom is chronic headache. It was speculated therefore that incidence of non-shunt related chronic headache in this group would be high, and an attempt was made to document incidence of migrainous and non-migrainous headache in the medical notes, and in replies to postal questionnaire sent to a sample of 130 children with shunted hydrocephalus of varying aetiology. Incidence of migrainous headache was documented in the medical notes in 8.5% of cases, with incidence rising to 21.5% using self-report. Incidence of non-migrainous headache was also very high (15.4%) and the overlap between migraine and tension headache, combined with difficulty of diagnosis in children may indicate migraine to be more frequent still. The concept of "Shunt Migraine" is therefore worthy of consideration. Report of chronic headache led to investigation in a large proportion of cases, but symptomatology often continued. Even when shunt malfunction was indicated, shunt revision did not "cure" complaint of headache. Headache was not found to be related to diagnosis associated with hydrocephalus, to presence of seizure disorder, or to the sex of the child, although in common with other studies, there was a strong trend towards girls being statistically more likely to experience headache than boys. There was a relationship however between report of chronic headache, and the sort of school a child was likely to attend; children who attended mainstream school without the support of a Statement of Special Educational Need were more likely to report headache than their peers, and it is hypothesised that these children may be suffering sufficient stress to contribute to maintenance of headache. The importance of the multi-disciplinary team in assessment of children's physical, intellectual and emotional status is stressed, in order that medical interventions have the greatest chance of success.

Investigative techniques and renal parenchymal damage in children with spina bifida.

The case records of 72 patients attending a multidisciplinary spina bifida clinic were reviewed to discover the prevalence of renal parenchymal damage. 19.4% of the total population had such damage. More detailed analysis of the group according to age showed that the prevalence of parenchymal damage in the over ten year olds (27.3%), was twice that of the under five year olds (13.3%) but the same as the prevalence of "at risk" patients (26.6%) in this group. On the basis that most renal parenchymal damage occurs early we conclude that the current approach to investigation and treatment is reducing the incidence of renal parenchymal damage in this population. Further reduction would require the early identification of the high risk bladder before the onset of hydronephrosis.

Isolation and characterization of a 70-kDa metalloprotease (gelatinase) that is elevated in Rous sarcoma virus-transformed chicken embryo fibroblasts.

Chicken embryo fibroblasts (CEF) transformed by Rous sarcoma virus (RSVCEF) secrete a 70-kDa metallo-gelatinase at elevated levels over that of normal CEF. The 70-kDa enzyme has been purified from RSVCEF conditioned medium and represents 1-3% of the total protein in the RSVCEF conditioned medium. A 22-kDa protein, which appears to be the avian form of the tissue inhibitor of metalloproteases (TIMP), is co-isolated in association with the 70-kDa enzyme and can be separated from the enzyme by gel filtration carried out under denaturing conditions. The isolated 70-kDa species is in the zymogen form. It can be activated by treatment with the organomercurial, p-aminophenylmercuric acetate (APMA), yielding a 62-kDa active species derived by an apparent autoproteolytic cleavage from the 70-kDa proenzyme as determined by both substrate gel analysis and immunoblots using a monospecific antibody to the 70-kDa proenzyme. The proenzyme is poorly activated by trypsin and not activated by plasmin. The APMA-activated enzyme rapidly degrades denatured collagens but under identical conditions is unable to degrade native collagens, including basement membrane type IV collagen. Only at very high enzyme to substrate ratios (1:2) will native type IV collagen be hydrolyzed. Partial N-terminal amino acid sequencing of both the 70-kDa proenzyme and the 62-kDa active enzyme indicates that the avian enzyme is a member of the matrix metalloprotease family (MMP-2). When CEF cultures, infected with a temperature sensitive mutant of RSV, conditional for the expression of the transforming src oncogene, were incubated at the permissive and nonpermissive temperatures, differential levels of the 70-kDa enzyme were produced in direct proportion to the functioning of the src oncogene.

Effects of prenatal stress and ethanol on cerebellar fiber tract maturation in B6D2F2 mice: an image analysis study.

Two studies were carried out to evaluate the role of prenatal stress in the outcome of prenatal ethanol exposure on central nervous system maturation in offspring. B6D2F1 mice were paid-fed liquid diets containing either 25% ethanol-derived calories or an isocaloric amount of maltose-dextrin on days 12 to 17 of gestation. During this period, half of the dams in each dietary condition also underwent two daily one-hour periods of restraint stress. A fifth group, provided with lab chow and water ad lib, was left undisturbed throughout pregnancy. At birth, all pups were fostered to untreated dams. Neither prenatal ethanol nor prenatal stress affected the maturation of cerebellar fiber tracts as indicated by membrane lipid staining either on day 32 post-conception or at weaning, nor was there an interactive effect of ethanol and stress combined. On the other hand, fiber tract maturation was significantly retarded on both days by prenatal undernutrition caused by treatment-induced reductions in maternal food intake. In the second study, pregnant dams were divided into three groups, all of which were fed lab chow and water. One group underwent the same stressing procedure as in the first study while a second group was unrestrained but pair-fed to the stressed group. A third group was undisturbed and allowed food and water ad lib. The offspring of both prenatally stressed and pair-fed dams did not differ from each other in terms of cerebellar fiber tract maturation, but both groups exhibited immature fiber tract development relative to the offspring of ad lib-fed dams. These data suggest that alterations in maternal nutritional status due to the ethanol and stress treatments can affect cerebellar fiber tract maturation in developing offspring.

Effects of prenatal ethanol and long-chain n-3 fatty acid supplementation on development in mice. 1. Body and brain growth, sensorimotor development, and water T-maze reversal learning.

Pregnant mice were fed equivalent daily amounts of a liquid diet containing 25% (kcal) ethanol, or with maltose dextrin substituted isocalorically for ethanol. In addition, the diet contained 20% oil; this was either of two mixtures, one comprised of predominantly n-6 (18:2n-6) fatty acids, and the other containing an equivalent amount of n-6, but supplemented with a source of long chain n-3 (20:5n-3, 22:6n-3) fatty acids. An additional control group was fed lab chow ad libitum. The treatment was implemented from day 7 to 17 of gestation, whereafter all groups were fed lab chow. Ethanol decreased maternal weight gain and pup body and brain weight; it also retarded both sensory and motor development in the pups and impeded reversal learning in a water maze. The n-3 supplementation lowered maternal blood alcohol concentration, but counteracted only some of the effects of ethanol, by increasing maternal weight gain and pup body weight, and also by enhancing sensory development in the pups. Such effects were additive, in that they were also present in the maltose-dextrin control group. These findings suggest that n-3 supplementation may ameliorate some of the effects of ethanol on neurobehavioral development, but the magnitude of the effect appears to be small.

Effects of prenatal ethanol and long-chain n-3 fatty acid supplementation on development in mice. 2. Fatty acid composition of brain membrane phospholipids.

Pregnant mice were fed equivalent daily amounts of a liquid diet containing 25% (kcal) ethanol, or with maltose dextrin substituted isocalorically for ethanol. The diet also contained 20% oil; this was either of two mixtures, one comprised of predominantly n-6 (18:2n-6) fatty acids, and the other containing an equivalent amount of n-6, but supplemented with a source of long chain n-3 (20:5n-3, 22:6n-3) fatty acids. An additional control group was fed lab chow ad libitum. The treatment was implemented from day 7 to 17 of gestation, whereafter all groups were fed lab chow. Birth occurred on day 19, and the fatty acid composition of the brain membrane phospholipids was determined in the pups 3 days after birth (day 22 postconception) and again, 10 days later (day 32 postconception). On day 22 the polyunsaturated fatty acid (PUFA) composition of the brain phospholipids reflected dietary availability, with the n-3/n-6 ratio higher in the n-3 groups; this was decreased by ethanol in the phosphatidylcholine (PC) fraction. The dietary effect was still apparent on day 32; again ethanol reduced this in both the PC and phosphatidylethanolamine (PE) fractions. The n-3 oil, but not ethanol, increased the 20:3n-6/20:4n-6 ratio, indicative of an inhibition of the activity of delta-5 desaturase. With respect to the 22:C compounds, the n-3 oil decreased the levels of 22:5n-6, while increasing those of 22:6n-3, but generally the sum of these two fatty acids remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Interactive effects of prenatal ethanol and N-3 fatty acid supplementation on brain development in mice.

This study assesses the combined effects on brain and behavioral development of ethanol administration and supplementation of the maternal diet with long chain n-3 polyunsaturated fatty acids. From day 7 to 17 of gestation, pregnant mice were fed equivalent daily amounts of isocaloric liquid diets; 20% of the energy was provided by either ethanol or maltose-dextrin, and a further 20% by either safflower oil (rich in linoleic acid, 18:2 n-6), or a combination of safflower oil with a fish oil concentrate (rich in eicosapentaenoic acid, 20:5 n-3, and docosahexaenoic acid, 22:6 n-3). On day 18 the liquid diets were replaced by lab chow; a fifth group was maintained on lab chow throughout the experiment. Measures on the pups included brain weight and the fatty acid composition of the brain phospholipids on days 22 and 32 post-conception (birth = day 19), as well as behavioral development. Maternal weight gain during gestation was decreased by ethanol relative to maltose-dextrin, and increased by fish relative to safflower oil. On day 32, the brain weight of ethanol-treated animals fed fish oil was greater than their safflower oil controls, whereas the reverse was true in the two maltose-dextrin groups; a similar trend was apparent on day 22. The brain phospholipid content of the longer chain fatty acids (20:4 n-6, 22:4 n-6, 22:5 n-6, 20:5 n-3, 22:5 n-3, 22:6 n-3) on day 22 reflected that of the prenatal diet, with the proportion of n-3 compounds being higher and that of n-6 lower in the fish oil than safflower oil groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Prenatal ethanol and stress in mice: 1. Pup behavioral development and maternal physiology.

On days 12 to 17 of pregnancy, B6D2F1 mice were pair-fed liquid diets containing either 25% ethanol-derived calories or an isocaloric amount of maltose-dextrin. During this period, half the mice in each dietary condition also underwent two daily one-hour periods of restraint stress. A fifth group, given lab chow and water ad lib, was left undisturbed throughout gestation. Neither treatment affected offspring body weight on days 22 or 32 postconception, but undernutrition produced by the pair feeding procedure reduced day 32 body weight in all groups relative to the ad lib-fed group. Both prenatal ethanol and pair feeding led to delayed neurobehavioral development on day 32, while prenatal stress significantly reduced the degree of developmental delay caused by these factors. In a second study, restraint stress significantly reduced blood alcohol concentrations in pregnant dams on day 15 of gestation while elevating plasma corticosterone concentrations, and this elevation was consistent regardless of the dietary condition of the dam. The pair feeding procedure also produced corticosterone elevations but the effect of ethanol was not significant. These results suggest that prenatal stress in the presence of other physiological insults may act to counter the actions of those insults.