Prenatal-through-postnatal exposure to moderate levels of ethanol leads to damage on the hippocampal CA1 field of juvenile rats

González-Burgos, Ignacio; Alejandre-Gómez, Misael; Olvera‐Cortés, María Esther; Vega, M.I. Pérez; Evans, Stephen M.; Feria‐Velasco, Alfredo

doi:10.1016/j.neures.2006.08.007

Cited by 42 publications

(33 citation statements)

References 57 publications

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“…While many studies have shown regional cell loss in the hippocampus following prenatal alcohol exposure [40], [59], [60], we did not find any differences in pyramidal cell number or density in the CA1 or CA3 regions of the dorsal hippocampus in ethanol exposed offspring. However, other studies have shown no difference in cell number and density within the CA1 and CA3 regions in neonatal (PN10) and adult (PN112) rat offspring exposed to moderate to high levels of alcohol during the gestational period equivalent to the first two trimesters of human pregnancy (G1-22/23), the same exposure period used in our study [61], [62].…”

Section: Discussioncontrasting

confidence: 99%

“…Previous research has demonstrated reductions in dendritic spine density as well as dendritic branching within the hippocampus, particularly within the CA1 region and the Dentate Gyrus [42], [43], [60]. We report a main effect of prenatal treatment for spine density within the CA3 region, suggesting an overall reduction in spine density for prenatal ethanol treated animals compared to control animals.…”

Section: Discussionsupporting

confidence: 48%

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Low Dose Prenatal Alcohol Exposure Does Not Impair Spatial Learning and Memory in Two Tests in Adult and Aged Rats

Cullen

Lavidis

2014

PLoS ONE

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Consumption of alcohol during pregnancy can have detrimental impacts on the developing hippocampus, which can lead to deficits in learning and memory function. Although high levels of alcohol exposure can lead to severe deficits, there is a lack of research examining the effects of low levels of exposure. This study used a rat model to determine if prenatal exposure to chronic low dose ethanol would result in deficits in learning and memory performance and if this was associated with morphological changes within the hippocampus. Sprague Dawley rats were fed a liquid diet containing 6% (vol/vol) ethanol (EtOH) or an isocaloric control diet throughout gestation. Male and Female offspring underwent behavioural testing at 8 (Adult) or 15 months (Aged) of age. Brains from these animals were collected for stereological analysis of pyramidal neuron number and dendritic morphology within the CA1 and CA3 regions of the dorsal hippocampus. Prenatal ethanol exposed animals did not differ in spatial learning or memory performance in the Morris water maze or Y maze tasks compared to Control offspring. There was no effect of prenatal ethanol exposure on pyramidal cell number or density within the dorsal hippocampus. Overall, this study indicates that chronic low dose prenatal ethanol exposure in this model does not have long term detrimental effects on pyramidal cells within the dorsal hippocampus or impair spatial learning and memory performance.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionsupporting

confidence: 48%

Low Dose Prenatal Alcohol Exposure Does Not Impair Spatial Learning and Memory in Two Tests in Adult and Aged Rats

Cullen

Lavidis

2014

PLoS ONE

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“…Our results in mice exposed to EtOH are consistent with other studies which have shown a decrease in dendritic complexity of MSNs from the NAc shell after gestational exposure (Rice et al , 2012), various subtypes of cortical neurons after gestational and/or postnatal exposure, (Hamilton et al , 2010a, Hamilton et al , 2010b, Lawrence et al , 2012) and a decrease in dendritic length in hippocampal CA1 neurons after exposure throughout gestation and postnatal development (Gonzalez-Burgos et al , 2006). In contrast, additional studies have failed to show a significant change in dendritic complexity of layer III apical dendrites of the mPFC (postnatal exposure; (Whitcher and Klintsova, 2008) or MSNs in the NAc (exposure throughout gestation and postnatal development; (Lawrence et al , 2012) and the dorsolateral or dorsomedial striatum (gestational exposure; (Rice et al , 2012).…”

Section: Discussionsupporting

confidence: 92%

Postnatal Ethanol Exposure Simplifies the Dendritic Morphology of Medium Spiny Neurons Independently of Adenylyl Cyclase 1 and 8 Activity in Mice

Susick

Lowing

Provenzano

et al. 2014

Alcoholism Clin & Exp Res

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Background Fetal exposure to alcohol can have multiple deleterious effects, including learning disorders and behavioral and executive functioning abnormalities, collectively termed fetal alcohol spectrum disorders. Neonatal mice lacking both calcium/calmodulin-stimulated adenylyl cyclases (ACs) 1 and 8 demonstrate increased vulnerability to ethanol-induced neurotoxicity in the striatum compared to wild type (WT) controls. However, the developmental impact on surviving neurons is still unclear. Methods WT and AC1/8 knock-out (DKO) mice were administered one dose of ethanol (2.5g/kg) between postnatal days 5-7 (P5-7). At P30, brains were removed and processed for Golgi-Cox staining. Medium spiny neurons (MSNs) from the caudate putamen were analyzed for changes in dendritic complexity; number of branches, branch points and terminals, total and average dendritic length; spine density, and soma size. Results Ethanol significantly reduced the dendritic complexity and soma size in surviving MSNs regardless of genotype without affecting spine density. In the absence of ethanol, genetic deletion of AC1/8 reduced the dendritic complexity, number of branch points, spine density and soma size of MSNs compared to WT controls. Conclusion These data indicate that neonatal exposure to a single dose of ethanol is sufficient to cause long-term alterations in the dendritic complexity of MSNs and that this outcome is not altered by the functional status of AC1 and AC8. Therefore, although deletion of AC1/8 demonstrates a role for the adenylyl cyclases in normal morphologic development and ethanol-induced neurodegeneration, loss of AC1/8 activity does not exacerbate the effects of ethanol on dendritic morphology or spine density.

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“…In humans, prenatal alcohol exposure alters hippocampal anatomy (for review see (Berman and Hannigan, 2000) and is associated with deficits in hippocampus-associated learning and memory (Mattson et al, 2001, Kooistra et al, 2010, Crocker et al, 2011, Mattson et al, 2011). Rodent work demonstrates that third trimester alcohol exposure leads to loss of hippocampal CA1 pyramidal cells, along with several pathological and plastic events in the dendritic arborization of these neurons (González-Burgos et al, 2006) as well as decreased cell numbers in the hippocampal CA1, CA3, and dentate gyrus regions (Livy et al, 2003). Further, third-trimester alcohol exposure leads to decreased neurogenesis in the adult hippocampal dentate gyrus (Hamilton et al, 2011, Hamilton et al, 2012) as well as impaired hippocampal functioning (Murawski and Stanton, 2010, Hamilton et al, 2011, Murawski et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Exercise and environment as an intervention for neonatal alcohol effects on hippocampal adult neurogenesis and learning

et al. 2014

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Neonatal alcohol exposure impairs cognition and learning in adulthood and permanently damages the hippocampus. Wheel running (WR) improves hippocampus-associated learning and memory and increases the genesis and survival of newly generated neurons in the hippocampal dentate gyrus. WR significantly increases proliferation of newly generated dentate granule cells in alcohol-exposed (AE) and control rats on Postnatal Day (PD) 42 but only control rats show an increased number of surviving cells thirty days after WR (Helfer et al., 2009b). The present studies examined whether proliferation-promoting WR followed by survival-enhancing environmental complexity (EC) during adolescence could increase survival of new neurons in AE rats. On PD4–9, pups were intubated with alcohol in a binge-like manner (5.25g/kg/day, AE), were sham-intubated (SI), or were reared normally (suckle control, SC). On PD30 animals were assigned to WR (PD30–42) followed by EC (PD42–72; WR/EC) or were socially housed (SH/SH) for the duration of the experiment. All animals were injected with 200 mg/kg BrdU on PD41. In Experiment 1, survival of newly generated cells was significantly enhanced in the AE-WR/EC group in comparison with AE-SH/SH group. Experiment 2A examined trace eyeblink conditioning. In the SH/SH condition, AE impaired trace eyeblink conditioning relative to SI and SC controls. In the WR/EC condition, AE rats performed as well as controls. In Experiment 2B, the same intervention was examined using the context preexposure facilitation effect (CPFE); a hippocampus-dependent variant of contextual fear conditioning. Again, the WR/EC intervention reversed the deficit in conditioned fear to the context that was evident in the SH/SH condition. Post-weaning environmental manipulations promote cell survival and reverse learning deficits in rats that were exposed to alcohol during development. These manipulations may provide a basis for developing interventions that ameliorate learning impairments associated with human fetal alcohol spectrum disorders.

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Prenatal-through-postnatal exposure to moderate levels of ethanol leads to damage on the hippocampal CA1 field of juvenile rats

Cited by 42 publications

References 57 publications

Low Dose Prenatal Alcohol Exposure Does Not Impair Spatial Learning and Memory in Two Tests in Adult and Aged Rats

Low Dose Prenatal Alcohol Exposure Does Not Impair Spatial Learning and Memory in Two Tests in Adult and Aged Rats

Postnatal Ethanol Exposure Simplifies the Dendritic Morphology of Medium Spiny Neurons Independently of Adenylyl Cyclase 1 and 8 Activity in Mice

Exercise and environment as an intervention for neonatal alcohol effects on hippocampal adult neurogenesis and learning

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