Dataset Information

Sleep electroencephalogram in children with a parental history of alcohol abuse/dependence.

ABSTRACT: We examined the sleep electroencephalogram (EEG) in 9- and 10-year-old children with (PH+) and without (PH-) a parental history of alcohol abuse/dependence to determine whether sleep disturbances associated with alcohol precede the onset of alcohol use. Participants slept on a fixed sleep schedule that ensured at least a 10-h time in bed for 1 week before an adaptation and baseline night. Data were collected in a four-bed sleep research laboratory. Thirty healthy boys and girls aged 9 or 10 years were classified as either PH+ or PH- based on DSM-IV criteria applied to structured parental interviews. All-night polysomnography was performed, sleep data were scored visually in 30-s epochs, and EEG power spectra were calculated for each epoch. All-night EEG spectra were calculated for rapid eye movement (REM) and non-REM (NREM) sleep, and cycle-by-cycle spectra were calculated for NREM sleep. The two groups did not differ on any sleep stage variable. All-night analyses revealed normalized power in the delta band and spindle range were lower in PH+ children. Within NREM sleep cycles PH+ children exhibited less normalized power in the delta band and spindle range compared with PH- children. This effect occurred in the first four cycles and was most pronounced in the first sleep cycle of the night. We found no signs of sleep disruption in sleep stages for PH+ children. Sleep EEG spectral differences, however, suggest that certain circuits responsible for 'protecting' sleep may be impaired in PH+ children, which may lead to disrupted sleep later in life.

SUBMITTER: Tarokh L

PROVIDER: S-EPMC2873133 | biostudies-literature | 2010 Mar

REPOSITORIES: biostudies-literature

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Sleep electroencephalogram in children with a parental history of alcohol abuse/dependence.

Tarokh Leila L Carskadon Mary A MA

Journal of sleep research 20090907 1 Pt 2

We examined the sleep electroencephalogram (EEG) in 9- and 10-year-old children with (PH+) and without (PH-) a parental history of alcohol abuse/dependence to determine whether sleep disturbances associated with alcohol precede the onset of alcohol use. Participants slept on a fixed sleep schedule that ensured at least a 10-h time in bed for 1 week before an adaptation and baseline night. Data were collected in a four-bed sleep research laboratory. Thirty healthy boys and girls aged 9 or 10 year ...[more]

PMID: 19735444

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Project description:Adolescent binge alcohol exposure has been previously shown to have long-lasting effects on the expression of hypothalamic genes that regulate the stress response, even in the absence of subsequent adult alcohol exposure. Those data suggested that alcohol can induce permanent gene expression changes, potentially through epigenetic modifications. Importantly, epigenetic modifications can be transmitted to future generations therefore, in these studies we investigated the effects of adolescent binge alcohol exposure on hypothalamic gene expression patterns in the F1 generation offspring. It has been well documented that maternal alcohol exposure during fetal development can have devastating neurological consequences. However, less is known about the consequences of maternal and/or paternal alcohol exposure outside of the gestational time frame. Here, we exposed adolescent male and female rats to a repeated binge EtOH exposure paradigm and then mated them in adulthood. Hypothalamic samples were taken from the offspring of these animals at postnatal day (PND) 7 and subjected to a genome-wide microarray analysis followed by qRT-PCR for selected genes. Importantly, the parents were not intoxicated at the time of mating and were not exposed to EtOH at any time during gestation therefore, the offspring were never directly exposed to EtOH. Our results showed that the offspring of alcohol-exposed parents had significant differences in the expression of hypothalamic genes that mediate neurogenesis and synaptic plasticity during neurodevelopment, genes important for directing chromatin remodeling, posttranslational modifications or transcription regulation, as well as genes involved in regulation of obesity and reproductive function. These data demonstrate that repeated binge alcohol exposure during pubertal development can potentially have detrimental effects on future offspring even in the absence of direct fetal alcohol exposure. Male and female Wistar rats were purchased from Charles River Laboratories (Wilmington, MA) at weaning (postnatal day (PND) 23) and allowed to acclimate for 7 days after arrival. Animals were handled for 5 min./once/day beginning at PND 30. Pubertal EtOH exposure began on PND 37, which is defined as peri-puberty. Animals were undisturbed following the first exposure of our binge EtOH exposure paradigm until PND 68 (late puberty/early adult) at which time they received a second exposure to the same treatment paradigm. During the duration of the experiment, males and females were separately housed in pairs on a 12:12 light/dark cycle with lights on at 0700 h with food and water available ad libitum. Binge Exposure Paradigm and Treatment Design. Rats were handled 5min./once/day for 7 d prior to treatment to control for nonspecific stress responses. At 37 d, animals were given 3 g/kg EtOH (20% v/v in tap water; N = 3/sex), or tap water alone (N = 3/sex), once/day via oral gavage at 10:00 AM to avoid disrupting normal feeding patterns. This process was repeated according to the following schedule for a total duration of 8 consecutive days: 3 d EtOH, 2 d tap water, 3 d EtOH. Control animals were given tap water alone once/day for 8 consecutive days. Our previous studies showed that this repeated binge-pattern EtOH paradigm does not affect body weight/growth curves and consistently results in blood alcohol concentrations (BAC) of 150-180 mg/dl in males and 210-240 mg/dl in females. We and others have previously used this paradigm as a model for the pattern of binge alcohol consumption observed in adolescents and BAC achieved are similar to those observed in humans following a binge drinking episode . After peri-pubertal treatments, animals were left undisturbed in their home cage until PND 68 when each group was again exposed to their respective treatment (i.e. control or binge EtOH. We waited 24 hours after the last dose of EtOH to ensure that blood alcohol concentrations in the parents were undetectable at the time of mating (data not shown). Animals were grouped into mating pairs: binge male + binge female (N = 3 pairs); water male + water female (N = 3 pairs). All of the females gave birth to 12-16 pups approximately 28 d after being housed with a male, indicating that conception took place approximately 6 d after pairing; therefore, the pups were never directly exposed to alcohol at any time. At PND 7 pups were deeply anesthetized on ice and sacrificed. Brains were rapidly removed, the hypothalamus microdissected on ice, and then stored in -80ºC until further processing for a genome-wide analysis on hypothalamic total RNA samples using a chip-based microarray (Southern California Genotyping Consortium, SCGC, Illumina Rat Ref-12). The PND 7 time point was chosen because the extent of rat neurodevelopment at PND 7 is roughly equivalent to that of a human infant at birth

Project description:Adolescent binge alcohol exposure has long-lasting effects on the expression of hypothalamic genes that regulate the stress response, even in the absence of subsequent adult alcohol exposure. This suggests that alcohol can induce permanent gene expression changes, potentially through epigenetic modifications to specific genes. Epigenetic modifications can be transmitted to future generations therefore, and in these studies we investigated the effects of adolescent binge alcohol exposure on hypothalamic gene expression patterns in the F1 generation offspring. It has been well documented that maternal alcohol exposure during fetal development can have devastating neurological consequences. However, less is known about the consequences of maternal and/or paternal alcohol exposure outside of the gestational time frame. Here, we exposed adolescent male and female rats to a repeated binge EtOH exposure paradigm and then mated them in adulthood. Hypothalamic samples were taken from the offspring of these animals at postnatal day (PND) 7 and subjected to a genome-wide microarray analysis followed by qRT-PCR for selected genes. Importantly, the parents were not intoxicated at the time of mating and were not exposed to EtOH at any time during gestation therefore the offspring were never directly exposed to EtOH. Our results showed that the offspring of alcohol-exposed parents had significant differences compared to offspring from alcohol-naïve parents. Specifically, major differences were observed in the expression of genes that mediate neurogenesis and synaptic plasticity during neurodevelopment, genes important for directing chromatin remodeling, posttranslational modifications or transcription regulation, as well as genes involved in regulation of obesity and reproductive function. These data demonstrate that repeated binge alcohol exposure during pubertal development can potentially have detrimental effects on future offspring even in the absence of direct fetal alcohol exposure.

Dataset Information

Sleep electroencephalogram in children with a parental history of alcohol abuse/dependence.

Publications

Sleep electroencephalogram in children with a parental history of alcohol abuse/dependence.

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