2017
DOI: 10.1002/brb3.636
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Acute ethanol exposure during late mouse neurodevelopment results in long‐term deficits in memory retrieval, but not in social responsiveness

Abstract: ObjectivePrenatal alcohol exposure can result in neurological changes in affected individuals and may result in the emergence of a broad spectrum of neurobehavioral abnormalities termed fetal alcohol spectrum disorders (FASD). The effects of ethanol exposure during development are both time and dose dependent. Although many animal models of FASD use more chronic ethanol exposure, acute developmental alcohol exposure may also cause long‐lasting neuronal changes. Our research employed behavioral measures to asse… Show more

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Cited by 15 publications
(5 citation statements)
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“…Our lab has investigated both social behavior and learning/memory in mice treated with this acute ethanol developmental paradigm. We found no overt social differences, but the animals exhibit memory deficits on the Barnes maze when learning acquisition occurs during adolescence and retention is tested in adulthood [ 7 , 53 ] This acquisition deficit fits well with our finding of PSD-95 abnormalities, as PSD-95 also appears to be important in coupling the NMDA receptor to pathways controlling synaptic plasticity and learning [ 28 ]..…”
Section: Discussionsupporting
confidence: 82%
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“…Our lab has investigated both social behavior and learning/memory in mice treated with this acute ethanol developmental paradigm. We found no overt social differences, but the animals exhibit memory deficits on the Barnes maze when learning acquisition occurs during adolescence and retention is tested in adulthood [ 7 , 53 ] This acquisition deficit fits well with our finding of PSD-95 abnormalities, as PSD-95 also appears to be important in coupling the NMDA receptor to pathways controlling synaptic plasticity and learning [ 28 ]..…”
Section: Discussionsupporting
confidence: 82%
“…C57BL6/J mice were exposed to a high acute ethanol dose on postnatal day 6 (P6) by dorsal subcutaneous injection of a 20% ethanol solution (2.5 g/kg dose) or saline control, followed by a second injection two hours later [ 7 ]. Pups were individually randomly assigned a treatment condition and were returned to their mothers between and after injections.…”
Section: Methodsmentioning
confidence: 99%
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“…The pattern of exposure, both binge-like (acute) and throughout the gestational period (chronic), has a noticeable effect on fetal neurodevelopment. While binge-like exposure incurs maximum damage to the developing fetus such as long-term memory deficits [ 69 ] and the altered expression of several developmental genes in the neonatal brain [ 70 , 71 ] as shown in several animal studies, chronic paternal exposure caused epigenetic dysregulation in the mouse neonates [ 72 ].…”
Section: Maternal Lifestylementioning
confidence: 99%
“…Voluntary drinking throughout gestation has produced a variety of behavioral impairments and deficits in tasks that tap into hippocampal function or sensorimotor integration with mixed data on activity (Allan et al, 2003; Becker et al, 1993; Brady et al, 2012; Downing et al, 2009; Fish et al, 2016; Sanchez Vega et al, 2013,). While fewer studies have assessed neonatal ETOH exposure on behavioral outcome in mice, Olney and colleagues have shown that a single postnatal ETOH injection can induce neuronal apoptosis (Ikonomidou et al, 2000) and may produce spatial deficits (Wozniak et al, 2004), although there are some inconsistencies in the literature (Lee et al, 2016, Houle et al, 2017). In addition, multiple injections of ETOH has been shown to alter performance on hippocampal and cerebellar tasks (Bearer et al, 2015, Wagner et al, 2014), although again hyperactivity is not uniformly reported (Downing et al, 2009).…”
Section: Introductionmentioning
confidence: 99%