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Postnatal Exposure (postnatal + exposure)
Selected AbstractsEarly Postnatal Exposure to Alcohol Reduces the Number of Neurons in the Occipital but Not the Parietal Cortex of the RatALCOHOLISM, Issue 4 2005Sandra M. Mooney Background: The rat brain undergoes a period of rapid growth in the early postnatal period. During this time, the neocortex seems to be vulnerable to ethanol injury. Subdivisions of the neocortex develop in a temporospatial gradient that is likely to determine their vulnerability to ethanol-induced damage and whether damage is permanent. Therefore, the authors investigated the effect of postnatal ethanol exposure on the neocortex and specific subregions at the cessation of exposure and in the mature brain. Methods: Four-day-old rat pups with intragastric cannulae were artificially reared from postnatal day (PN) 4 through PN9. Of 12 daily feeds, two consecutive feeds contained either ethanol (4.5 g/kg) or an isocaloric maltose/dextrin solution. On PN10 or PN115, animals were perfused intracardially, and the brains were removed. Stereological methods were used to determine the total number of neurons and glial cells in, and the volume of, the neocortex, the parietal cortex, and the occipital cortex. Results: Exposure to ethanol did not affect body or brain weight at PN10. In contrast, at PN115 forebrain weight was significantly lower in ethanol-exposed animals compared with control-treated animals. There was no effect of treatment on body weight at PN115. On PN10, neocortical volume was 15% smaller in the ethanol-exposed animals compared with controls, with no change in the total number of neurons or glial cells. Occipital cortical volume was reduced by 22% in the ethanol-exposed animals, with a significant deficit in the total number of neurons (ethanol-exposed, 2.62 × 106; gastrostomy control, 3.20 × 106). There was no effect of ethanol exposure on the total number of glial cells in the occipital cortex or on any parameter in the parietal cortex. There was also no significant effect of ethanol exposure on the occipital cortex on PN115. Conclusions: These findings provide support for the hypothesis that a specific area or cell population might be differentially vulnerable to ethanol exposure during the brain growth spurt and that cell deficits evident on PN10 may not be permanent. [source] Lead-induced alterations of apoptosis and neurotrophic factor mRNA in the developing rat cortex, hippocampus, and cerebellumJOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, Issue 5 2007Shirley L. Chao Abstract Previous reports have recently shown the prototypic neurotoxicant, lead, to induce apoptosis in the brains of developing organisms. In the current study, timed-pregnant rats were exposed to lead acetate (0.2% in the drinking water) 24 h following birth at postnatal day 1 (PND 1). Dams and pups were continuously exposed to lead through the drinking water of the dam until PND 20. Postnatal exposure in the pups resulted in altered mRNA levels of the following apoptotic and neurotrophic factors: caspase 2 and 3, bax, bcl-x, brain-derived neurotrophic factor (BDNF). Ribonuclease protection assays were conducted to measure the factors simultaneously at the following postnatal time points: 9, 12, 15, 20, 25, days. Our results suggest a brain region- and time-specific response following lead acetate exposure. The region most vulnerable to alterations occurs in the hippocampus with alterations beginning at PND 12, in which caspase 3, bcl-x, BDNF increase with lead exposure. Significant treatment effects were not observed for both the cortex and cerebellum. © 2007 Wiley Periodicals, Inc. J Biochem Mol Toxicol 21:265,272, 2007; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20191 [source] Nicotine in breast milk influences heart rate variability in the infantACTA PAEDIATRICA, Issue 8 2008Anders Dahlström Abstract Aim: To study the effects of postnatal exposure to nicotine on the regulation of heart rate and blood pressure in infants. Subjects and Methods: Thirty-eight mother,infant pairs were studied. Twenty nonsmoking and 18 smoking (2,20 cigarettes per day) mothers were included. All infants were healthy, exclusively breastfed and their postnatal age was 6 weeks. During a home visit infant's urine and mothers' milk were sampled and concentrations of nicotine and cotinine were analyzed. Infants' electrocardiogram (ECG) were recorded, sleep state documented and blood pressure during sleep was measured. Heart rate variability (HRV) was calculated with spectral analysis of R,R intervals. Results: The smoking mothers exposed their infants to nicotine in milk with a median nicotine concentration of 47 (8,192) ,g/L. Analysis of infants' urine showed that the nonsmoking group had 0.8 (0,5.2) and the smoke group 60 (17,139) ,g cotinine/L (p < 0.01). The frequency domain low-to-high frequency (LF/HF) ratio, was correlated to milk nicotine concentrations in the milk sample, from smoking mothers. HRV decreased, with increasing milk nicotine, ingested by the boys (r =,0.74, p = 0.02) but not the girls (r =,0.13, p = 0.76). The differences of mean arterial pressure between sleep states in the infants, were significantly lower in the smoke group 5.8(6.8) compared to the nonsmoke group 11.5(7.2) mmHg (p = 0.03). Conclusions: Postnatal exposure to nicotine influences autonomic cardiovascular control in infants. [source] The Interaction of Gestational and Postnatal Ethanol Experience on the Adolescent and Adult Odor-Mediated Responses to Ethanol in Observer and Demonstrator RatsALCOHOLISM, Issue 10 2010Amber M. Eade Background:, Gestational ethanol exposure enhances the adolescent reflexive sniffing response to ethanol odor. Postnatal exposures of naïve animals as either an observer (i.e., conspecific) or demonstrator (i.e., intoxicated peer) using a social transmission of food odor preference paradigm also yields enhanced odor-mediated responses. Studies on the interaction of fetal and postnatal exposures using the social transmission paradigm have been limited to the responses of observers. When combined, the enhanced response is greater than either form of exposure alone and, in observer females, yields adult persistence. The absence of a male effect is noteworthy, given that chemosensory mechanisms are suggested to be an important antecedent factor in the progression of ethanol preference. Observers gain odor information on the breath of the demonstrator through social interaction. Demonstrators experience the pharmacologic properties of ethanol along with retronasal and hematogenic olfaction. Thus, we tested whether augmentation of the fetal ethanol-induced behavioral response with postnatal exposure as a demonstrator differed from that as an observer. We also examined whether re-exposure as a demonstrator yields persistence in both sexes. Methods:, Pregnant dams were fed an ethanol containing or control liquid diet throughout gestation. Progeny received four ethanol or water exposures: one every 48 hours through either intragastric infusion or social interaction with the infused peer beginning on P29. The reflexive behavioral sniffing response to ethanol odor was tested at postnatal (P) day 37 or P90, using whole-body plethysmography. Results:, When tested in either adolescence or adulthood - fetal ethanol exposed adolescent ethanol observers and demonstrators significantly differed in their odor-mediated response to ethanol odor both between themselves and from their respective water controls. Nonetheless, adolescent ethanol re-exposure as a demonstrator, like an observer, enhanced the reflexive sniffing response to ethanol odor at both testing ages by augmenting the known effects of prior fetal ethanol experience. At each age, the magnitude of the enhanced odor response in demonstrators was similar to that of observers. Interestingly, only re-exposure as a demonstrator resulted in persistence of the behavioral response into adulthood in both sexes. Conclusions:, The method of ethanol re-exposure plays an important role in prolonging the odor-mediated effects of fetal exposure. While ethanol odor-specific exposure through social interaction is important, additional factors such as the pairing of retronasal and hematogenic olfaction with ethanol's intoxicating properties appear necessary to achieve persistence in both sexes. [source] Oestrogen imprinting causes nuclear changes in epithelial cells and overall inhibition of gene transcription and protein synthesis in rat ventral prostateINTERNATIONAL JOURNAL OF ANDROLOGY, Issue 5 2010T. M. Augusto Summary Oestrogen exposure during the early post-natal period affects male growth, physiology, and susceptibility to disease in adult life. The prostate gland is susceptible to this oestrogen imprinting, showing a reduced expression of the androgen receptor and inability to respond to androgen stimulus. In this context, we decided to study key signalling regulators of ventral prostate (VP) functioning after early postnatal exposure to high-dose oestrogen. Our results showed a decrease of mTOR phosphorylation and its direct downstream target 4EBP. It is known that mTOR-induced signalling is a pivotal pathway of cell metabolism, which is able to control gene transcription and protein synthesis. We then decided to investigate other indicators of a reduced metabolism in the oestrogenized prostate, and found that the luminal epithelial cells were shorter, less polarized and had smaller nuclei containing more compacted chromatin, suggesting that a general mechanism of regulating gene expression and protein synthesis could be installed in the epithelium of the oestrogenized VP. To evaluate this idea, we analysed nucleolar morphology, and measured the amount of ribosomes and the level of methylation of the 45S ribosomal RNA promoter region. These data indicated that the nucleolus was dismantled and that the methylation at the 45S promoter was increased (,five-fold). Taken together, the results support the idea that the oestrogenized prostate maintains a very low transcriptional level and protein turnover by affecting canonical signalling pathways and promoting nuclear and nucleolar changes. [source] The Interaction of Gestational and Postnatal Ethanol Experience on the Adolescent and Adult Odor-Mediated Responses to Ethanol in Observer and Demonstrator RatsALCOHOLISM, Issue 10 2010Amber M. Eade Background:, Gestational ethanol exposure enhances the adolescent reflexive sniffing response to ethanol odor. Postnatal exposures of naïve animals as either an observer (i.e., conspecific) or demonstrator (i.e., intoxicated peer) using a social transmission of food odor preference paradigm also yields enhanced odor-mediated responses. Studies on the interaction of fetal and postnatal exposures using the social transmission paradigm have been limited to the responses of observers. When combined, the enhanced response is greater than either form of exposure alone and, in observer females, yields adult persistence. The absence of a male effect is noteworthy, given that chemosensory mechanisms are suggested to be an important antecedent factor in the progression of ethanol preference. Observers gain odor information on the breath of the demonstrator through social interaction. Demonstrators experience the pharmacologic properties of ethanol along with retronasal and hematogenic olfaction. Thus, we tested whether augmentation of the fetal ethanol-induced behavioral response with postnatal exposure as a demonstrator differed from that as an observer. We also examined whether re-exposure as a demonstrator yields persistence in both sexes. Methods:, Pregnant dams were fed an ethanol containing or control liquid diet throughout gestation. Progeny received four ethanol or water exposures: one every 48 hours through either intragastric infusion or social interaction with the infused peer beginning on P29. The reflexive behavioral sniffing response to ethanol odor was tested at postnatal (P) day 37 or P90, using whole-body plethysmography. Results:, When tested in either adolescence or adulthood - fetal ethanol exposed adolescent ethanol observers and demonstrators significantly differed in their odor-mediated response to ethanol odor both between themselves and from their respective water controls. Nonetheless, adolescent ethanol re-exposure as a demonstrator, like an observer, enhanced the reflexive sniffing response to ethanol odor at both testing ages by augmenting the known effects of prior fetal ethanol experience. At each age, the magnitude of the enhanced odor response in demonstrators was similar to that of observers. Interestingly, only re-exposure as a demonstrator resulted in persistence of the behavioral response into adulthood in both sexes. Conclusions:, The method of ethanol re-exposure plays an important role in prolonging the odor-mediated effects of fetal exposure. While ethanol odor-specific exposure through social interaction is important, additional factors such as the pairing of retronasal and hematogenic olfaction with ethanol's intoxicating properties appear necessary to achieve persistence in both sexes. [source] Primary sensitization to inhalant allergensPEDIATRIC ALLERGY AND IMMUNOLOGY, Issue 2000Claudia Macaubas The neonatal T-cell system is capable of responding to allergens at birth, indicating the occurrence of prenatal sensitization, and the cytokine profile of these responses is skewed towards the Th-2 type. This response is further modified by postnatal exposure to different types of allergens. In relation to inhalant allergen (employed by HDM) the low level fetal Th-2 responses in non-atopics appear to be down-regulated rapidly after birth, parallel to an increase in allergen-specific IFN-, production. In contrast, atopics appear to consolidate their initial Th-2 responses, and around the age of 6 exhibit a cytokine response profile similar to the adult pattern. A pre-existing deficiency in IFN-, production may be one of the key factors determining the postnatal persistence of Th-2 responses in atopics. [source] Lack of adverse effects in pregnant/lactating female rats and their offspring following pre- and postnatal exposure to ELF magnetic fieldsBIOELECTROMAGNETICS, Issue 4 2004Moon-Koo Chung Abstract We have recently reported that exposure of pregnant rats to 60 Hz at field strengths up to 0.5 mT during the entire period of pregnancy did not induce any biologically significant effects on both pregnant dams and embryo-fetal development. The present study was carried out to investigate the potential effects of gestational and lactational MF exposure on pregnancy, delivery, and lactation of dams and growth, behavior, and mating performance of their offspring in rats. Timed-pregnant female Sprague,Dawley (SD) rats (24/group) received continuous exposure to 60 Hz magnetic field (MF) at field strengths of 0 (sham control), 5 ,T, 83.3 ,T, or 0.5 mT. Dams received MF or sham exposures for 21 h/day from gestational day 6 through lactational day 21. Experimentally generated MF was monitored continuously throughout the study. No exposure-related changes in clinical signs, body weight, food consumption, pregnancy length, and necropsy findings were observed in dams. Parameters of growth, behavior, and reproductive performance of offspring showed no changes related to MF exposure. There were no adverse effects on embryo-fetal development of F2 offspring from dams exposed to MF. In conclusion, exposure of pregnant SD rats to 60 Hz at field strengths up to 0.5 mT from gestational day 6 to lactational day 21 did not produce biologically significant effects in dams, F1 offspring, or F2 fetuses. Bioelectromagnetics 25:236,244, 2004. © 2004 Wiley-Liss, Inc. [source] Prenatal and postnatal parental smoking and acute otitis media in early childhoodACTA PAEDIATRICA, Issue 1 2010SE Håberg Abstract Aim:, To explore the associations between acute otitis media in early childhood and prenatal and postnatal tobacco smoke exposure. Methods:, Subjects were 32 077 children born between 2000 and 2005 in the Norwegian Mother and Child Study with questionnaire data on tobacco smoke exposure and acute otitis media up to 18 months of age. Multivariate regression models were used to obtain adjusted relative risks for acute otitis media. Results:, Acute otitis media was slightly more common in children exposed to parental smoking. The incidence from 0 to 6 months was 4.7% in unexposed children and 6.0% in children exposed both prenatally and postnatally. After adjusting for postnatal exposure and covariates, the relative risk for acute otitis media 0,6 months when exposed to maternal smoking in pregnancy was 1.34, 95% confidence interval: 1.06,1.69. Maternal smoking in pregnancy was associated with acute otitis media up to 12 months of age. Compared with non-exposed children, there was a slightly increased risk of recurrent acute otitis media for children exposed both prenatally and postnatally with a relative risk of 1.24, 95% confidence interval: 1.01,1.52. Conclusion:, Even in a cohort with relatively low exposure levels of parental smoking, maternal smoking in pregnancy was associated with an increased risk of acute otitis media in early childhood. [source] Exposure to secondhand tobacco smoke and child behaviour , results from a cross-sectional study among preschool children in BavariaACTA PAEDIATRICA, Issue 1 2010D Twardella Abstract Aim:, To evaluate the association of postnatal exposure to secondhand tobacco smoke on childhood behavioural problems after taking maternal smoking during pregnancy into account. Methods:, In a cross-sectional survey of preschool children in Bavaria, exposure to secondhand tobacco smoke in the child's home was assessed via a parent questionnaire. The Strength and Difficulties Questionnaire (SDQ) was applied to assess child's behaviour. The association with secondhand tobacco smoke exposure was assessed for ,probable' outcomes of the problem subscales and of prosocial behaviour. Results:, Among 5494 children (48% female), the SDQ indicated behavioural problems in up to 11%. After adjustment for socioeconomic factors, low birth weight and maternal smoking before and during pregnancy, a dose-response relationship with exposure to secondhand tobacco smoke was observed regarding hyperactivity/inattention (odds ratio compared to ,none' was 1.35 for ,low/medium' and 2.39 for ,high' exposure, 95% confidence intervals 1.02,1.78 and 1.62,3.53, respectively) as well as for conduct problems (OR 1.68 (1.37,2.06) and 1.93 (1.39,2.68)). Conclusion:, Secondhand tobacco smoke exposure at home appears to be associated with an increased risk of behavioural problems among preschool children. Prevention of behavioural problems may be a further reason to target secondhand tobacco smoke exposure in children. [source] Nicotine in breast milk influences heart rate variability in the infantACTA PAEDIATRICA, Issue 8 2008Anders Dahlström Abstract Aim: To study the effects of postnatal exposure to nicotine on the regulation of heart rate and blood pressure in infants. Subjects and Methods: Thirty-eight mother,infant pairs were studied. Twenty nonsmoking and 18 smoking (2,20 cigarettes per day) mothers were included. All infants were healthy, exclusively breastfed and their postnatal age was 6 weeks. During a home visit infant's urine and mothers' milk were sampled and concentrations of nicotine and cotinine were analyzed. Infants' electrocardiogram (ECG) were recorded, sleep state documented and blood pressure during sleep was measured. Heart rate variability (HRV) was calculated with spectral analysis of R,R intervals. Results: The smoking mothers exposed their infants to nicotine in milk with a median nicotine concentration of 47 (8,192) ,g/L. Analysis of infants' urine showed that the nonsmoking group had 0.8 (0,5.2) and the smoke group 60 (17,139) ,g cotinine/L (p < 0.01). The frequency domain low-to-high frequency (LF/HF) ratio, was correlated to milk nicotine concentrations in the milk sample, from smoking mothers. HRV decreased, with increasing milk nicotine, ingested by the boys (r =,0.74, p = 0.02) but not the girls (r =,0.13, p = 0.76). The differences of mean arterial pressure between sleep states in the infants, were significantly lower in the smoke group 5.8(6.8) compared to the nonsmoke group 11.5(7.2) mmHg (p = 0.03). Conclusions: Postnatal exposure to nicotine influences autonomic cardiovascular control in infants. [source] The Interaction of Gestational and Postnatal Ethanol Experience on the Adolescent and Adult Odor-Mediated Responses to Ethanol in Observer and Demonstrator RatsALCOHOLISM, Issue 10 2010Amber M. Eade Background:, Gestational ethanol exposure enhances the adolescent reflexive sniffing response to ethanol odor. Postnatal exposures of naïve animals as either an observer (i.e., conspecific) or demonstrator (i.e., intoxicated peer) using a social transmission of food odor preference paradigm also yields enhanced odor-mediated responses. Studies on the interaction of fetal and postnatal exposures using the social transmission paradigm have been limited to the responses of observers. When combined, the enhanced response is greater than either form of exposure alone and, in observer females, yields adult persistence. The absence of a male effect is noteworthy, given that chemosensory mechanisms are suggested to be an important antecedent factor in the progression of ethanol preference. Observers gain odor information on the breath of the demonstrator through social interaction. Demonstrators experience the pharmacologic properties of ethanol along with retronasal and hematogenic olfaction. Thus, we tested whether augmentation of the fetal ethanol-induced behavioral response with postnatal exposure as a demonstrator differed from that as an observer. We also examined whether re-exposure as a demonstrator yields persistence in both sexes. Methods:, Pregnant dams were fed an ethanol containing or control liquid diet throughout gestation. Progeny received four ethanol or water exposures: one every 48 hours through either intragastric infusion or social interaction with the infused peer beginning on P29. The reflexive behavioral sniffing response to ethanol odor was tested at postnatal (P) day 37 or P90, using whole-body plethysmography. Results:, When tested in either adolescence or adulthood - fetal ethanol exposed adolescent ethanol observers and demonstrators significantly differed in their odor-mediated response to ethanol odor both between themselves and from their respective water controls. Nonetheless, adolescent ethanol re-exposure as a demonstrator, like an observer, enhanced the reflexive sniffing response to ethanol odor at both testing ages by augmenting the known effects of prior fetal ethanol experience. At each age, the magnitude of the enhanced odor response in demonstrators was similar to that of observers. Interestingly, only re-exposure as a demonstrator resulted in persistence of the behavioral response into adulthood in both sexes. Conclusions:, The method of ethanol re-exposure plays an important role in prolonging the odor-mediated effects of fetal exposure. While ethanol odor-specific exposure through social interaction is important, additional factors such as the pairing of retronasal and hematogenic olfaction with ethanol's intoxicating properties appear necessary to achieve persistence in both sexes. [source] | ||||||||||