Influence of Fetal Alcohol Exposure on the GABAergic Regulation of Growth Hormone Release in Postnatal Rats

Blaine, Kelly M.; Gasser, Kenneth W.; Conway, Sonya

doi:10.1111/j.1530-0277.1999.tb04061.x

Cited by 4 publications

(2 citation statements)

References 65 publications

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“…Although there was no significant effect of FAE, it may be of future interest to further elucidate the GABAergic system relative to the catecholaminergic neurons in the PVN. Previous studies had shown an effect of FAE on the GABAergic system in relation to the HPG axis (Blaine et al, 1999) and the GABA A receptor (Allan et al, 1998), where there was decreased sensitivity of GABA A receptor stimulation in FAE males but not females. Also, after moderate exposure to alcohol during gestation, adult FAE rats displayed altered sensitivity to the GABA A receptors in the prefrontal cortex, hippocampus, and cerebellum.…”

Section: Discussionmentioning

confidence: 98%

Novel role of adrenergic neurons in the brain stem in mediating the hypothalamic–pituitary axis hyperactivity caused by prenatal alcohol exposure

2008

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Exposure to alcohol during embryonic development leads to changes in the hypothalamicpituitary-adrenal (HPA) axis such that adult offspring release more adrenocorticotrophic hormone (ACTH) than controls when exposed to stress. In the present work, we tested the hypothesis that changes in the activity of the catecholaminergic system modulate, at least in part, this upregulation of the HPA axis. Pregnant Sprague Dawley rats were exposed to alcohol 6 hours daily during gestation days 7-18 using the vapour chamber model, which generated mean blood alcohol levels of 188.6 ± 10 mg/dl. All experiments were performed on 2-3 month-old offspring. We measured the ACTH response to intracerebroventricular injection of adrenergic receptor agonists. In rats exposed to footshocks, we investigated the activity of corticotrophin-releasing factor (CRF) as well as indexes of catecholamine immunoreactivity, namely tyrosine hydroxylase (TH) immunopositive neurons in the paraventricular nucleus (PVN), TH immunopositive neurons in the locus coeruleus, and phenylethanolamine N-methyltransferase (PNMT) immunopositive neurons in the brain stem. While adult females exposed to alcohol during fetal development (FAE) displayed the expected enhanced ACTH response to stress, there were no significant differences in response to adrenergic receptor agonists or in shock-induced CRF/TH immunoreactivity (ir) and neuronal activity, as determined by c-fos colocalization. In contrast, FAE female offspring exposed to footshocks showed a significant increase in the activity of adrenergic neurons in the C1 region of the brain stem, a population of cells that project to the PVN. Collectively, these results suggest that while FAE-induced hyperactivity of the HPA axis is not accompanied by significant changes in CRF or TH-ir neurons, it is characterized by an upregulation of C1 adrenergic neurons of the brain stem. This novel finding should lead to the functional characterization of this brain region in the FAE model.

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Section: Discussionmentioning

confidence: 98%

Novel role of adrenergic neurons in the brain stem in mediating the hypothalamic–pituitary axis hyperactivity caused by prenatal alcohol exposure

2008

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“…Among these are an impairment of growth hormone, LH and FSH release, increased stress-induced release of glucocorticoids, decreases in thyroxine, reduced prenatal and postnatal surge of testosterone, poor thermoregulation and shorter reproductive life spans in females. (Blaine et al, 1999, Handa et al, 1985, Lee et al, 2000, McGivern et al, 1988, 1995Scott et al, 1998, Taylor et al, 1982a, Weinberg et al, 1996, Wilcoxon and Redei, 2004, Zimmerberg et al, 1993. Disruptions in behaviors regulated by the hypothalamus are also observed in FAE (Fetal Alcohol Exposed) animals, including decreased maternal behavior in females, decreased reproductive behavior in males, feminization of taste preferences in males and increased daily water consumption (Barron and Riley, 1985, Hard et al, 1984, McGivern et al, 1984.…”

Section: Introductionmentioning

confidence: 99%

Prenatal ethanol exposure alters core body temperature and corticosterone rhythms in adult male rats

Zuloaga

McGivern

2007

Alcohol

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Ethanol's effects on the developing brain include alterations in morphology and biochemistry of the hypothalamus. To examine the potential functional consequences of ethanol's interference with hypothalamic differentiation, we studied the long-term effects of prenatal ethanol exposure on basal circadian rhythms of core body temperature (CBT) and heart rate (HR). We also examined the late afternoon surge in corticosterone (CORT). Core body temperature and HR rhythms were studied in separate groups of animals at 4, 8, and 20 months of age. The normal late afternoon rise in plasma CORT was examined in freely moving male rats at 6 months of age via an indwelling right atrial cannula. Results showed that the CBT circadian rhythm exhibited an earlier rise after the nadir of the rhythm in fetal alcohol-exposed (FAE) males at all ages compared to controls. At 8 months of age, the amplitude of the CBT circadian rhythm in FAE males was significantly reduced to the level observed in controls at 20 months. No significant effects of prenatal ethanol exposure were observed on basal HR rhythm at any age. The diurnal rise in CORT secretion was blunted and prolonged in 6-month-old FAE males compared to controls. Both control groups exhibited a robust surge in CORT secretion around the onset of the dark phase of the light cycle, which peaked at 7:30 p.m. Whereas FAE males exhibited a linear rise beginning in mid afternoon, which peaked at 9:30 p.m. These results indicate that exposure to ethanol during the period of hypothalamic development can alter the long-term regulation of circadian rhythms in specific physiological systems.

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Strain-specific programming of prenatal ethanol exposure across generations

Popoola

Nizhnikov

Cameron

2017

Alcohol

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Behavioral consequences of prenatal alcohol exposure (PAE) can be transmitted from in utero-exposed F1 generation to their F2 offspring. This type of transmission is modulated by genetic and epigenetic mechanism. This study investigated the intergenerational consequences of prenatal exposure to low ethanol dose (1g/kg) during gestational days 17–20, on ethanol-induced hypnosis in adolescent male F1 and F2 generations, in two strains of rats. Adolescent Long Evans and Sprague Dawley male rats were tested for sensitivity to ethanol-induced hypnosis at 3.5g/kg or 4.5g/kg ethanol dose using the loss of righting reflex (LORR) paradigm. We hypothesized that PAE would attenuate sensitivity to ethanol-induced hypnosis in the ethanol-exposed animals in these two strains and in both generations. Interestingly, we only found this effect in Sprague Dawley rats. Lastly, we investigated PAE related changes in expression of GABAA receptor α1, α4, and δ subunits in the cerebral cortex of the PAE sensitive Sprague Dawley strain. We hypothesized a reduction in the cerebral cortex GABAA receptor subunits’ expression in the F1 and F2 PAE groups compared to control animals. GABAA receptor α1, α4, and δ subunits protein expressions were quantified in the cerebral cortex of F1 and F2 male adolescents by western blotting. PAE didn’t alter cerebral cortical GABAA receptor subunit expressions in the F1 generation, but it decreased GABAA receptor α4 and δ subunits’ expressions in the F2 generation, and had a tendency to decrease α1 subunit expression. We also found correlations between some of the subunits in both generations. These strain-dependent vulnerabilities to ethanol sensitivity, and intergenerational PAE-mediated changes in sensitivity to alcohol indicate that genetic and epigenetic factors interact to determine the outcomes of PAE animals and their offspring.

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Influence of Fetal Alcohol Exposure on the GABAergic Regulation of Growth Hormone Release in Postnatal Rats

Cited by 4 publications

References 65 publications

Novel role of adrenergic neurons in the brain stem in mediating the hypothalamic–pituitary axis hyperactivity caused by prenatal alcohol exposure

Novel role of adrenergic neurons in the brain stem in mediating the hypothalamic–pituitary axis hyperactivity caused by prenatal alcohol exposure

Prenatal ethanol exposure alters core body temperature and corticosterone rhythms in adult male rats

Strain-specific programming of prenatal ethanol exposure across generations

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