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Adult Offspring (adult + offspring)
Selected AbstractsDose-Dependent Effects of Prenatal Ethanol Exposure on Synaptic Plasticity and Learning in Mature OffspringALCOHOLISM, Issue 11 2002Daniel D. Savage Background We have observed profound deficits in hippocampal synaptic plasticity and one-trial learning in offspring whose mothers drank moderate quantities of ethanol during pregnancy. In the present study, we examined the question of whether lower maternal blood ethanol concentrations (BECs) could produce functional deficits in offspring. Methods Rat dams consumed either a 2%, 3%, or 5% ethanol liquid diet throughout gestation. Three other groups of dams were pair-fed a 0% ethanol liquid diet, and a seventh group consumed lab chow ad libitum. Adult offspring from each diet group were assigned either to studies of evoked [3H]-D-aspartate (D-ASP) release from hippocampal slices or spatial learning studies using the Morris Water Task. Results Consumption of the 2%, 3%, and 5% ethanol liquid diets produced mean peak maternal BECs of 7, 30 and 83 mg/dL, respectively. Consumption of these ethanol diets had no effect on offspring birthweight, litter size or neonatal mortality. Likewise, evoked D-ASP release from hippocampal slices and performance on a standard version of the Morris Water Task were not affected by prenatal ethanol exposure. By contrast, activity-dependent potentiation of evoked D-ASP release from slices and one-trial learning on a "moving platform" version of the Morris Water Task were markedly reduced in offspring whose mothers consumed the 5% ethanol liquid diet. Intermediate deficits in these two parameters were observed in offspring from the 3% ethanol diet group, whereas offspring from the 2% ethanol diet group were not statistically different than controls. Conclusions We conclude that the threshold for eliciting subtle, yet significant learning deficits in offspring prenatally exposed to ethanol is less than 30 mg/dL. This BEC is roughly equivalent to drinking 1 to 1.5 ounces of ethanol per day. [source] Psychological functioning and health-related quality of life in adulthood after preterm birthDEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 8 2007Stuart R Dalziel FRACP PhD The aim of this study was to determine if preterm birth is associated with socioeconomic status (SES), psychological functioning, and health-related quality of life (HRQoL) in adulthood. We used prospective follow-up of 192 adult offspring of mothers who took part in a randomized controlled trial of antenatal betamethasone for the prevention of neonatal respiratory distress syndrome (66 born at term [33 males, 33 females] 126 born preterm [66 males, 60 females]). Cognitive functioning was assessed using the Wechsler Abbreviated Scale of Intelligence. Working memory and attention was assessed using the Benton Visual Retention Test, the Paced Auditory Serial Addition Test, and the Brown Attention Deficit Disorder Scale. Psychiatric morbidity was assessed using the Beck Depression Inventory II, the State-Trait Anxiety Inventory, and the Schizotypy Traits Questionnaire. Handedness was assessed using the Edinburgh Handedness Inventory. HRQoL was assessed using the Short Form-36 Health Survey. Moderately preterm birth (median gestation 34wks, mean birthweight 1946g [SD 463g]) was not related to later marital status, educational attainment, SES, cognitive functioning, working memory, attention, or symptoms of anxiety or schizotypy at 31 years of age. Preterm birth was associated with fewer symptoms of depression and higher levels of satisfaction in three of the eight HRQoL domains measured (bodily pain, general health perception, and social functioning). Adults who were born moderately preterm have SES, psychological functioning, and HRQoL consistent with those who were born at term. This good long-term outcome cannot be extrapolated to those with early childhood disability or very low birthweights. [source] The familial aggregation of cannabis use disordersADDICTION, Issue 4 2009Kathleen R. Merikangas ABSTRACT Aims The aim of this paper is to examine the familial aggregation of cannabis use disorders and other psychiatric conditions among first-degree relatives and spouses of probands with a cannabis use disorder. Design Controlled family study methods. Setting Out-patient psychiatric clinics and the local community (same geographic area). Participants Two hundred and sixty-two probands with a life-time history of cannabis use disorder, alcohol dependence, anxiety disorders or no history of any disorder, and their first-degree relatives and spouses. Measurements Cannabis use disorders and other DSM-III-R disorders in the relatives and spouses using the Schedule for Affective Disorders and Schizophrenia. Findings Results reveal an elevated risk of life-time history of cannabis use disorders among siblings [odds ratio (OR: 3.6), adult offspring (OR): 6.9], and spouses (OR: 4.4) of probands with cannabis use disorders. There is a latent familial factor underlying cannabis use disorders that was shared partially with alcohol abuse/dependence. Comorbid mood and anxiety disorders aggregated independently from cannabis use disorders in families. Equal elevation in the magnitude of the association among the first-degree adult relatives and spouses of probands with a cannabis use disorder suggests the probable contribution of both environmental and genetic factors. Conclusions These findings support a family-based approach to drug abuse intervention and the importance of future research concerning environmental mediators of familial transmission of drug abuse. [source] Prenatal stress reduces postnatal neurogenesis in rats selectively bred for high, but not low, anxiety: possible key role of placental 11,-hydroxysteroid dehydrogenase type 2EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 1 2009P. J. Lucassen Abstract Prenatal stress (PS) produces persistent abnormalities in anxiety-related behaviors, stress responsivity, susceptibility to psychopathology and hippocampal changes in adult offspring. The hippocampus shows a remarkable degree of structural plasticity, notably in response to stress and glucocorticoids. We hypothesized that PS would differentially affect hippocampal neurogenesis in rats selectively bred for genetic differences in anxiety-related behaviors and stress responsivity. Pregnant dams of high anxiety-related behavior (HAB) and low anxiety-related behavior (LAB) strains were stressed between days 5 and 20 of pregnancy. The survival of newly generated hippocampal cells was found to be significantly lower in 43-day-old HAB than in LAB male offspring of unstressed pregnancies. PS further reduced newly generated cell numbers only in HAB rats, and this was paralleled by a reduction in doublecortin-positive cell numbers, indicative of reduced neurogenesis. As maternal plasma corticosterone levels during PS were similar in both strains, we examined placental 11,-hydroxysteroid dehydrogenase type 2 (11,-HSD2), which catalyses rapid inactivation of maternal corticosterone to inert 11-dehydrocorticosterone and thus serves as a physiological ,barrier' to maternal glucocorticoids. PS significantly increased placental 11,-HSD2 activity in LAB, but not HAB, rats. We conclude that PS differentially affects the number of surviving newly generated cells and neurogenesis in HAB and LAB rats. The high sensitivity of hippocampal neurogenesis to PS in HAB rats is paralleled by a failure to increase placental 11,-HSD2 activity after stress rather than by different maternal corticosterone responses. Hence, stress-induced placental 11,-HSD2 expression may be critical in protecting the fetal brain from maternal stress-induced effects on adult neurogenesis. [source] Do Parental Stressors and Avoidance Coping Mediate Between Parental Depression and Offspring Depression?FAMILY RELATIONS, Issue 2 2010A 23-Year Follow-Up We examined whether parents' stressors and avoidance coping when offspring were children helped to explain associations between parent depression at baseline and offspring's avoidance coping and depression in adulthood. Self-report data were collected at baseline and 1 year from parents (N = 326) and at 23 years from adult offspring (N = 326). Associations between parents' depression symptoms at baseline, and their adult offspring's depression symptoms and avoidance coping 23 years later, were partially explained by parents' reliance on avoidance coping in response to negative events at 1 year after baseline. [source] Maternal high-fat feeding primes steatohepatitis in adult mice offspring, involving mitochondrial dysfunction and altered lipogenesis gene expression,HEPATOLOGY, Issue 6 2009Kimberley D. Bruce Nonalcoholic fatty liver disease (NAFLD) describes an increasingly prevalent spectrum of liver disorders associated with obesity and metabolic syndrome. It is uncertain why steatosis occurs in some individuals, whereas nonalcoholic steatohepatitis (NASH) occurs in others. We have generated a novel mouse model to test our hypothesis: that maternal fat intake contributes to the development of NAFLD in adult offspring. Female mice were fed either a high-fat (HF) or control chow (C) diet before and during gestation and lactation. Resulting offspring were fed either a C or a HF diet after weaning, to generate four offspring groups; HF/HF, HF/C, C/HF, C/C. At 15 weeks of age, liver histology was normal in both the C/C and HF/C offspring. Kleiner scoring showed that although the C/HF offspring developed nonalcoholic fatty liver, the HF/HF offspring developed NASH. At 30 weeks, histological analysis and Kleiner scoring showed that both the HF/C and C/HF groups had NAFLD, whereas the HF/HF had a more severe form of NASH. Therefore, exposure to a HF diet in utero and during lactation contributes toward NAFLD progression. We investigated the mechanisms by which this developmental priming is mediated. At 15 weeks of age, hepatic mitochondrial electron transport chain (ETC) enzyme complex activity (I, II/III, and IV) was reduced in both groups of offspring from HF-fed mothers (HF/C and HF/HF). In addition, measurement of hepatic gene expression indicated that lipogenesis, oxidative stress, and inflammatory pathways were up-regulated in the 15-week-old HF/C and HF/HF offspring. Conclusion: Maternal fat intake contributes toward the NAFLD progression in adult offspring, which is mediated through impaired hepatic mitochondrial metabolism and up-regulated hepatic lipogenesis. (HEPATOLOGY 2009.) [source] Developmental toxicity of UV filters and environmental exposure: a reviewINTERNATIONAL JOURNAL OF ANDROLOGY, Issue 2 2008Margret Schlumpf Summary Several ultraviolet (UV) filters exhibit estrogenic, some also anti-androgenic activity. They are present in waste water treatment plants, surface waters and biosphere including human milk, suggesting potential exposure during development. Developmental toxicity was studied in rats for the UV filters 4-methylbenzylidene camphor (4-MBC, 0.7, 7, 24, 47 mg/kg/day) and 3-benzylidene camphor (3-BC, 0.07, 0.24, 0.7, 2.4, 7 mg/kg/day) administered in chow to the parent generation before mating, during pregnancy and lactation, and to the offspring until adulthood. Neonates exhibited enhanced prostate growth after 4-MBC and altered uterine gene expression after both chemicals. 4-MBC and 3-BC delayed male puberty and affected reproductive organ weights of adult offspring. Effects on the thyroid axis were also noted. Expression and oestrogen sensitivity of oestrogen-regulated genes and nuclear receptor coregulator levels were altered at mRNA and protein levels in adult uterus, prostate and brain regions involved in gonadal control and sexual behaviour. Female sexual behaviour was impaired by both filters; 3-benzylidene camphor caused irregular cycles. Classical endpoints exhibited lowest observed adverse effect levels (LOAELs) and no observed adverse effect levels (NOAELs) of 7/0.7 mg/kg for 4-MBC and 0.24/0.07 mg/kg for 3-BC. Molecular endpoints were affected by the lowest doses studied. Our data indicate that the potential risk posed by endocrine active UV filters warrants further investigations. [source] Educational Attainments of Immigrant Offspring: Success or Segmented Assimilation?,INTERNATIONAL MIGRATION REVIEW, Issue 4 2002Monica Boyd In this article, I study the educational attainments of the adult offspring of immigrants, analyzing data from the 1996 panel of the Survey of Labour and Income Dynamics (SLID). Fielded annually since 1993 by Statistics Canada, respondents are asked for the first time in 1996 to report the birthplaces of their parents, making it possible to define and study not only the foreign-born population (the first generation), but also the second generation (Canadian born to foreign-born parents) and the third-plus generation (Canadian born to Canadian-born parents). The survey also asked respondents to indicate if they are members of a visible minority group, thus permitting a limited assessment of whether or not color conditions educational achievements of immigrant offspring. I find that "1.5" and second generation adults, age 20,64 have more years of schooling and higher percentages completing high school compared with the third-plus generation. Contrary to the segmented "underclass" assimilation model found in the United States, adult visible minority immigrant offspring in Canada exceed the educational attainments of other not-visible-minority groups. Although the analysis is hampered by small sample numbers, the results point to country differences in historical and contemporary race relations, and call for additional national and cross-national research. [source] Parents of Adults with Intellectual Disabilities: Quality of Life and Experiences of CaringJOURNAL OF APPLIED RESEARCH IN INTELLECTUAL DISABILITIES, Issue 2 2000Sarah Walden This study examined a UK sample of parents caring for their adult offspring with intellectual disabilities, and the factors contributing to their quality of life and experiences of caregiving. Structured interviews were conducted with 62 parents of adults with intellectual disabilities. On several indices of quality of life, parents did not seem to be functioning as well as caregiving parents in the US, or as well as adults in the general US population. The offspring's level of challenging behaviour and physical dependency and the parent's satisfaction with informal support were associated with parental quality of life. The salience that parents placed on their post-parental life style was also associated with quality of life, with ,captive' parents faring more poorly than ,captivated' parents. [source] Fetal and offspring arrhythmia following exposure to nicotine during pregnancyJOURNAL OF APPLIED TOXICOLOGY, Issue 1 2010Yu Feng Abstract Although recent studies have demonstrated prenatal nicotine can increase cardiovascular risk in the offspring, it is unknown whether exposure to nicotine during pregnancy also may be a risk for development of arrhythmia in the offspring. In addition, in previous studies of fetal arrhythmia affected by smoking, only two patterns, bradycardia and tachycardia, were observed. The present study examined acute effects of maternal nicotine on the fetal arrhythmia in utero, and chronic influence on offspring arrhythmia at adult stage following prenatal exposure to nicotine. Nicotine was administered to pregnant ewes and rats. In the fetal sheep, intravenous nicotine not only induced changes of fetal heart rate, but also caused cardiac cycle irregularity, single and multiple dropped cardiac cycles. Although maternal nicotine had no influence on fetal blood pH, lactic acid, hemocrit, Na+, K+ levels and plasma osmolality, fetal blood PO2 levels were significantly decreased following maternal nicotine in ewes. In offspring rats at 4,5 months after birth, prenatal exposure to nicotine significantly increased heart rate and premature ventricular contraction in restraint stress. In addition, arrhythmias induced by injection of nicotine were higher in the offspring prenatal exposure to nicotine in utero. The results provide new evidence that exposure to nicotine in pregnancy can cause fetal arrhythmia in various patterns besides tachycardia and bradycardia, the possible mechanisms for nicotine-induced fetal arrhythmia included in utero hypoxia. Importantly, following exposure to nicotine significantly increased risk of arrhythmia in the adult offspring. The finding offers new insight for development of cardiac rhythm problems in fetal origins. Copyright © 2009 John Wiley & Sons, Ltd. [source] Altered Mesencephalic Dopaminergic Populations in Adulthood as a Consequence of Brief Perinatal Glucocorticoid ExposureJOURNAL OF NEUROENDOCRINOLOGY, Issue 8 2005S. McArthur Abstract Early exposure to stressors is strongly associated with enduring effects on central nervous system function, but the mechanisms and neural substrates involved in this biological ,programming' are unclear. This study tested the hypothesis that inappropriate exposure to glucocorticoid stress hormones (GCs) during critical periods of development permanently alters the mesencephalic dopaminergic populations in the ventral tegmental area (VTA) and substantia nigra pars compacta (SNc). Using a rat model, the synthetic GC dexamethasone was added to the maternal drinking water during gestational days 16,19 or over the first week of postnatal life. In adulthood, the effects upon tyrosine hydroxylase immunopositive (TH+) cell numbers in the midbrain, and monoamine levels in the forebrain, of the adult offspring were assessed and compared with control offspring whose dams received normal drinking water. In the VTA, both prenatal and postnatal dexamethasone treatment increased TH+ cell numbers by approximately 50% in males and females. Although prenatal dexamethasone treatment also increased TH+ cell numbers in the SNc by 40,50% in males and females, postnatal treatment affected females only by increasing TH+ cell numbers by approximately 30%. In comparison, similar changes were not detected in the monoamine levels of the dorsolateral striatum, nucleus accumbens or infralimbic cortex of either males or females, which is a feature likely to reflect adaptive changes in these pathways. These studies demonstrate that the survival or phenotypic expression of VTA and SNc dopaminergic neurones is profoundly influenced by brief perinatal exposure to GCs at times when endogenous levels are normally low. These findings are the first to demonstrate permanent changes in the cytoarchitecture within midbrain dopamine nuclei after perinatal exposure to stress hormones and implicate altered functionality. Thus, they have significance for the increasing use of GCs in perinatal medicine and indicate potential mechanisms whereby perinatal distress may predispose to the development of a range of psychiatric conditions in later life. [source] Naturally Occurring Differences in Maternal Care are Associated with the Expression of Oxytocin and Vasopressin (V1a) Receptors: Gender DifferencesJOURNAL OF NEUROENDOCRINOLOGY, Issue 5 2002D. D. Francis Abstract Variations in maternal care have been associated with long-term changes in neurochemistry and behaviour in adult rats. Rats receiving high levels of licking and grooming as pups are less fearful and more maternal than rats receiving low levels of maternal licking and grooming. Central pathways for oxytocin and vasopressin have been implicated in the neurobiology of anxiety and social behaviours. We assessed whether variations in maternal care were associated with differences in oxytocin receptors (OTR) or vasopressin (V1a) receptors in the brains of adult offspring. In the central nucleus of the amygdala and bed nucleus of the stria terminalis, OTR binding was increased in adult females, but not adult males, that had received high levels of maternal licking and grooming as pups. Conversely, amygdala V1a receptor binding was increased in males, but not females, that had received high levels of maternal licking and grooming. These findings suggest that variations in maternal care may influence the expression of oxytocin and vasopressin receptors in a gender-specific manner. [source] Effects of a Novel Cognition-Enhancing Agent on Fetal Ethanol-Induced Learning DeficitsALCOHOLISM, Issue 10 2010Daniel D. Savage Background:, Drinking during pregnancy has been associated with learning disabilities in affected offspring. At present, there are no clinically effective pharmacotherapeutic interventions for these learning deficits. Here, we examined the effects of ABT-239, a histamine H3 receptor antagonist, on fetal ethanol-induced fear conditioning and spatial memory deficits. Methods and Results:, Long-Evans rat dams stably consumed a mean of 2.82 g ethanol/kg during a 4-hour period each day during pregnancy. This voluntary drinking pattern produced a mean peak serum ethanol level of 84 mg/dl. Maternal weight gain, litter size and birth weights were not different between the ethanol-consuming and control groups. Female adult offspring from the control and fetal alcohol-exposed (FAE) groups received saline or 1 mg ABT-239/kg 30 minutes prior to fear conditioning training. Three days later, freezing time to the context was significantly reduced in saline-treated FAE rats compared to control. Freezing time in ABT-239-treated FAE rats was not different than that in controls. In the spatial navigation study, adult male offspring received a single injection of saline or ABT-239 30 minutes prior to 12 training trials on a fixed platform version of the Morris Water Task. All rats reached the same performance asymptote on Trials 9 to 12 on Day 1. However, 4 days later, first-trial retention of platform location was significantly worse in the saline-treated FAE rats compared control offspring. Retention by ABT-239-treated FAE rats was similar to that by controls. ABT-239's effect on spatial memory retention in FAE rats was dose dependent. Conclusions:, These results suggest that ABT-239 administered prior to training can improve retention of acquired information by FAE offspring on more challenging versions of hippocampal-sensitive learning tasks. Further, the differential effects of ABT-239 in FAE offspring compared to controls raises questions about the impact of fetal ethanol exposure on histaminergic neurotransmission in affected offspring. [source] Maternal smoking during pregnancy predicts nicotine disorder (dependence or withdrawal) in young adults , a birth cohort studyAUSTRALIAN AND NEW ZEALAND JOURNAL OF PUBLIC HEALTH, Issue 4 2009Frances V. O'Callaghan Abstract Objective: To investigate whether maternal smoking during pregnancy predicts offspring nicotine disorder (dependence or withdrawal) at 21 years. Method: Participants comprised a prospective birth cohort involving 7,223 singleton children whose mothers were enrolled between 1981 and 1983 at the first antenatal visit to the Mater Mothers' Hospital, Brisbane, Queensland. The present sub-cohort consisted of 2,571 youth who completed the Composite International Diagnostic Interview-computerised version (CIDI-Auto) that assesses nicotine dependence and withdrawal according to DSM-IV diagnostic criteria at the 21-year follow-up. Results: 12.8% of offspring met criteria for nicotine dependence and 8.5% met criteria for withdrawal. 16.6% met criteria for either dependence or withdrawal. Smoking during pregnancy resulted in offspring being more likely to have dependence or withdrawal at 21 years than offspring of mothers who never smoked (age adjusted odds ratio 1.53 (95% CI: 1.19-1.96). Conclusions: Findings emphasise the long-term adverse effects of maternal smoking during pregnancy, including nicotine dependence in young adult offspring. Implications: Public health approaches should strengthen arguments for mothers to cease smoking during pregnancy in view of the long-term health implications for offspring, and reinforce measures to help smokers among pregnant women and women of childbearing age to stop. [source] | |||||||||||||