Alcohol consumption during pregnancy among Southern city women

Stephens, Cheryl J.

doi:10.1016/0376-8716(85)90078-x

Cited by 51 publications

(19 citation statements)

References 6 publications

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“…Both ethanol and control exposure periods were 2 h, 30 min each day. This acute exposure protocol mimics a "binge" pattern of ethanol consumption, which is a common consumption pattern in women who drink during pregnancy (Stephens, 1985).…”

Section: Ethanol Vapor Inhalation Exposure Paradigmmentioning

confidence: 99%

Influence of ethanol on neonatal cerebellum of BDNF gene‐deleted animals: analyses of effects on Purkinje cells, apoptosis‐related proteins, and endogenous antioxidants

et al. 2002

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The sensitivity of the developing central nervous system (CNS) to the deleterious effects of ethanol has been well documented, with exposure leading to a wide array of CNS abnormalities. Certain CNS regions are susceptible to ethanol during well-defined critical periods. In the neonatal rodent cerebellum, a profound loss of Purkinje cells is found when ethanol is administered early in the postnatal period [on postnatal days 4 or 5 (P4-5)], while this neuronal population is much less vulnerable to similar ethanol insult slightly later in the postnatal period (P7-9). Prior studies have shown that neurotrophic factors (NTFs) can be altered by ethanol exposure, and both in vitro and in vivo studies have provided evidence that such substances have the potential to protect against ethanol neurotoxicity. In the present study, it was hypothesized that depletion of an NTF shown to be important to cerebellar development would exacerbate ethanol-related effects within this region, when administration was confined to a normally ethanol-resistant ontogenetic period. For this study, brain-derived neurotrophic factor (BDNF) gene-deleted ("knockout") and wild-type mice were exposed to ethanol via vapor inhalation or to control conditions during the normally ethanol-resistant period (P7 and P8). Two hours after termination of exposure on P8, analyses were made of body weight, crown-rump length, and brain weight. In subsequent investigations, the number and density of Purkinje cells and the volume of cerebellar lobule I were determined, and the expression of anti- and pro-apoptotic proteins and the activities of endogenous antioxidants were assessed. It was found that the BDNF knockouts were significantly smaller than the wild-type animals, with smaller brain weights. Purkinje cell number and density was reduced in ethanol-treated knockout, but not wild-type animals, and the volume of lobule I was significantly decreased in the gene-deleted animals compared to wild-types, but was not further affected by ethanol treatment. The loss of Purkinje cells in the BDNF knockouts was accompanied by decreases in anti-apoptotic Bcl-xl and in phosphorylated (and hence inactivated) pro-apoptotic Bad, and reduced activity of the antioxidant glutathione reductase, while the antioxidant catalase was increased by ethanol treatment in this genotype. In the wild-type animals, anti-apoptotic Bcl-2 was decreased by ethanol treatment, but the pro-apoptotic c-Jun N-terminal kinase (JNK) was markedly diminished by ethanol exposure, while the activity of the protective antioxidant superoxide dismutase (SOD) was significantly enhanced. These results suggest that neurotrophic factors have the capacity to protect against ethanol neurotoxicity, perhaps by regulation of expression of molecules critical to neuronal survival such as elements of the apoptosis cascade and protective antioxidants.

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Section: Ethanol Vapor Inhalation Exposure Paradigmmentioning

confidence: 99%

Influence of ethanol on neonatal cerebellum of BDNF gene‐deleted animals: analyses of effects on Purkinje cells, apoptosis‐related proteins, and endogenous antioxidants

et al. 2002

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“…When heavy alcohol consumption does continue into the 3rd trimester (coinciding with part of the so-called brain growth spurt in humans) (Dobbing & Sands, 1979), the severity of fetal alcohol effects is generally increased (Rosett et al, 1983;Rosett, Weiner, Zuckerman, McKinlay, & Edelin, 1980;Smith et al, 1986). Furthermore, women who abuse alcohol in the last trimester of pregnancy often engage in intermittent episodes of binge drinking (Stephens, 1985), a pattern associated with increased risk of brain damage and behavioral deficits (Goodlett, Bonthius, Wasserman, & West, 1992;Streissguth et al, 1989;West, Goodlett, Bonthius, & Pierce, 1989). Whether the timing of binge episodes during the 3rd trimester brain growth spurt determines the extent of CNS damage and behavioral dysfunction is essentially unknown.…”

Section: Introductionmentioning

confidence: 98%

Behavioral deficits induced by bingelike exposure to alcohol in neonatal rats: Importance of developmental timing and number of episodes

et al. 1996

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“…Correspondence concerning tbis article should be addressed to Derick H. Lindquist, Departments of Psycbology & Neuroscienee, Tbe Obio State University, 1835 Neil Ave., Room 45,Columbus,.edu known to produce higher peak BACs than chronically consumed alcohol (Bonthius et al, 1988) and better mimics the consumption patterns of alcoholic pregnant women (Stephens, 1985). Alcohol's teratogenic effects on forebrain development, the medial prefrontal cortex and hippocampus in particular, can be seen via reduced cell numbers (Livy et al, 2003;Mihalick et al, 2001) and constrained or altered spine density and dendritic complexity (Hamilton et al, 2010;Tanaka et al, 1991).…”

mentioning

confidence: 94%

Impaired trace fear conditioning and diminished ERK1/2 phosphorylation in the dorsal hippocampus of adult rats administered alcohol as neonates.

DuPont

Coppola

Kaercher

et al. 2014

Behavioral Neuroscience

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Utilizing a rat model of fetal alcohol spectrum disorder (FASD), ethanol was administered over postnatal days (PD) 4 to 9. As adults, control and ethanol rats underwent trace fear conditioning (TFC), in which a tone conditioned stimulus (CS) and footshock unconditioned stimulus (US) were repeatedly paired, though the two stimuli never overlapped in time. Following training in Experiment 1, conditioned fear (freezing) to the tone CS was dose-dependently reduced in ethanol rats relative to controls. Experiment 2 was designed to test whether the TFC deficit varied based on the duration of the trace interval (TI; time from CS offset to US onset). Holding the time separating CS onset from US onset constant at 20 sec, control and ethanol rats were trained with a 5 or 15 sec tone CS, followed 15 or 5 sec later, respectively, by the US. Conditioned fear to the tone CS was significantly reduced in high dose ethanol rats trained with the 15 sec TI only. Acquisition and consolidation of trace fear memories relies on forebrain N-methyl-d-aspartate receptor (NMDAR) signaling, including the downstream phosphorylation of extracellular signal-regulated kinase 1/2 (pERK1/2). Separate rats were trained with the 5 or 15 sec TI and then sacrificed 1 hr later. Significant reductions in pERK1/2-positive neurons were seen in areas CA1 and CA3 of the dorsal hippocampus (DH) following training at both TIs in ethanol rats. The disruption of DH learning-dependent plasticity appears tied to freezing behavior in ethanol rats, but only when the training stimuli are separated by more than 5 sec.

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Alcohol consumption during pregnancy among Southern city women

Cited by 51 publications

References 6 publications

Influence of ethanol on neonatal cerebellum of BDNF gene‐deleted animals: analyses of effects on Purkinje cells, apoptosis‐related proteins, and endogenous antioxidants

Influence of ethanol on neonatal cerebellum of BDNF gene‐deleted animals: analyses of effects on Purkinje cells, apoptosis‐related proteins, and endogenous antioxidants

Behavioral deficits induced by bingelike exposure to alcohol in neonatal rats: Importance of developmental timing and number of episodes

Impaired trace fear conditioning and diminished ERK1/2 phosphorylation in the dorsal hippocampus of adult rats administered alcohol as neonates.

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