Morphological recovery of hippocampal pyramidal neurons in the adult rat exposed in utero to ethanol

Ferrer, Isidró; Galofré, F.; López-Tejero, Dolores; Llobera, Miquel

doi:10.1016/0300-483x(88)90100-x

Cited by 25 publications

(9 citation statements)

References 10 publications

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“…Some other authors also did not find an adverse effect of gestational ethanol on the composition and levels of the PSD‐95 associated NMDA receptor complexes (Hughes et al, 2001; Samudio‐Ruiz et al, 2010). These results remain in contradiction to other studies reporting reduction in spine density (Ferrer et al, 1988) and changes in ligand binding, subunit expression, and function of NMDA receptors after perinatal ethanol exposure (for review see Costa et al, 2000). However, the discrepancies in the obtained results may arise from differences in ethanol doses applied and the peak BAC, as well as the way, duration, and timing of ethanol administration with respect to the developmental critical periods.…”

Section: Discussioncontrasting

confidence: 99%

Investigation into the effects of prenatal alcohol exposure on postnatal spine development and expression of synaptophysin and PSD95 in rat hippocampus

Elibol-Can

Kılıç

Yürüker

et al. 2013

Intl J of Devlp Neuroscience

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Ethanol is known as a potent teratogen responsible for the fetal alcohol syndrome characterized by cognitive deficits especially pronounced in juveniles but ameliorating in adults. Since the mechanisms of these deficits and following partial recovery are not fully elucidated, the aim of the present study was to investigate the process of synaptogenesis in the hippocampus over the first two months of life in control and fetal‐alcohol rats. Ethanol was delivered to the pregnant dams by intragastric intubation throughout 7–21 gestation days at the daily dose of 6 g/kg generating a mean blood alcohol level of 246.6 ± 40.9 mg/dl on gestation day 20. The spine densities as well as the expression of pre‐ and postsynaptic proteins, synaptophysin (SYP) and PSD‐95 protein, were evaluated for three distinct hippocampal regions: CA1, CA2+3, and DG and four postnatal days: PD1, PD10, PD30 and PD60, independently. Our results confirmed an intensive synaptogenesis within the brain spurt period (first 10 postnatal days), however, the temporal pattern of changes in the SYP and PSD‐95 expression was different. The ethanol exposure during half of the 1st and the whole 2nd human trimester equivalent resulted in an overall trend toward lower values of synaptic indices at PD1 with a fast recovery from these deficits observed already at PD10. At PD30, around the age when the most pronounced behavioral deficits have been previously reported in juvenile fetal‐alcohol subjects, no significant changes were found in either the hippocampal levels of synaptic proteins or in the spine density in principal hippocampal neurons.

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Section: Discussioncontrasting

confidence: 99%

Investigation into the effects of prenatal alcohol exposure on postnatal spine development and expression of synaptophysin and PSD95 in rat hippocampus

Elibol-Can

Kılıç

Yürüker

et al. 2013

Intl J of Devlp Neuroscience

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“…The adverse effect of ethanol on the neurite growth can also arise from its interaction with GABA receptors which, at the early stages of brain development, have excitatory properties (Rogers and Hunter, 1992) and elevate the intracellular Ca 2+ (Prendergast et al, 2004), damping the dendrite growth and branching (Kostyuk, 1986;Mameli et al, 2005). Ethanol was also reported by other authors to reduce the spine density both in vivo (Ferrer et al, 1988;Kuge et al, 1993), and in vitro (Yanni and Lindsley, 2000) and cause changes in the shape of dendritic spines in hippocampal neurons in the rat (Tarelo-Acuña et al, 2000). The fact that sometimes the effects of the developmental ethanol intoxication and stress exposure overlap and sometimes they are unique may arise from different sensitivity of different parameters to the potentially adverse factors across the postnatal ages.…”

Section: Effects Of the Exposure To Fetal Alcohol And Maternal Stressmentioning

confidence: 82%

Effects of prenatal binge‐like ethanol exposure and maternal stress on postnatal morphological development of hippocampal neurons in rats

Jakubowska-Doğru

Elibol

Dursun

et al. 2017

Intl J of Devlp Neuroscience

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This study showed regional and temporal differences in the development of different morphometric features of principal hippocampal neurons in intact subjects over a protracted 2-months postnatal period. It also demonstrated an overlap in the effects of a moderate fetal ethanol intoxication and a mild maternal stress produced by the intragastric intubation, a commonly used method of ethanol administration to the pregnant dams. Fast recovery from the adverse effects on the soma size, dendritic arborization and spines density observed at birth indicates towards the fetal ethanol/stress induced developmental retardation.

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“…Further, dendritic morphology, spine numbers and shape are dynamic with the ability to change rapidly or remain stable for prolonged periods (Holtmaat et al, 2005). Several studies have failed to find ethanol-induced differences in spine density and morphology using the Golgi procedure (Pentney et al, 1984, Galofre et al, 1987, Ferrer et al, 1988). It should be noted that these studies used manual quantification which may have resulted in more error in the findings.…”

Section: Discussionmentioning

confidence: 99%

Selective effects of perinatal ethanol exposure in medial prefrontal cortex and nucleus accumbens

Lawrence

Otero

Kelly

2012

Neurotoxicology and Teratology

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Ethanol exposure during development is the leading known cause of mental retardation and can result in characteristic physiological and cognitive deficits, often termed Fetal Alcohol Spectrum Disorders (FASD). Previous behavioral findings using rat models of FASD have suggested that there are changes in the nucleus accumbens (NAC) and medial prefrontal cortex (mPFC) following ethanol exposure during development. This study used a rat model of FASD to evaluate dendritic morphology in both the NAC and mPFC and cell number in the NAC. Dendritic morphology in mPFC and NAC were assessed using a modified Golgi stain and analyzed via three dimensional reconstructions with Neurolucida (MBF Bioscience). Cell counts in the NAC (shell and core) were determined using an unbiased stereology procedure (Stereo Investigator (MBF Bioscience)). Perinatal ethanol exposure did not affect neuronal or glial cell population numbers in the NAC. Ethanol exposure produced a sexually dimorphic effect on dendritic branching at one point along the NAC dendrites but was without effect on all other measures of dendritic morphology in the NAC. In contrast, spine density was reduced and distribution was significantly altered in layer II/III neurons of the mPFC following ethanol exposure. Ethanol exposure during development was also associated with an increase in soma size in the mPFC. These findings suggest that previously observed sexually dimorphic changes in activation of the NAC in a rat model of FASD may be due to altered input from the mPFC.

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Morphological recovery of hippocampal pyramidal neurons in the adult rat exposed in utero to ethanol

Cited by 25 publications

References 10 publications

Investigation into the effects of prenatal alcohol exposure on postnatal spine development and expression of synaptophysin and PSD95 in rat hippocampus

Investigation into the effects of prenatal alcohol exposure on postnatal spine development and expression of synaptophysin and PSD95 in rat hippocampus

Effects of prenatal binge‐like ethanol exposure and maternal stress on postnatal morphological development of hippocampal neurons in rats

Selective effects of perinatal ethanol exposure in medial prefrontal cortex and nucleus accumbens

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