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Postnatal ethanol exposure impairs social behavior and operant extinction in the adult female mouse offspring
被引:1
|作者:
Bariselli, Sebastiano
[1
]
Reuveni, Noa
[1
]
Westcott, Nina
[1
]
Mateo, Yolanda
[1
]
Lovinger, David M.
[1
]
机构:
[1] Natl Inst Alcohol Abuse & Alcoholism, Lab Integrat Neurosci LIN, Bethesda, MD 20892 USA
基金:
美国国家卫生研究院;
关键词:
late-term gestational ethanol exposure;
social behavior;
anhedonia;
extinction;
anxiety-like behaviors;
ALCOHOL SPECTRUM DISORDERS;
FETAL ALCOHOL;
PRENATAL EXPOSURE;
ELEVATED PLUS;
RATS;
CHILDREN;
ANXIETY;
STRESS;
BRAIN;
VULNERABILITY;
D O I:
10.3389/fnins.2023.1160185
中图分类号:
Q189 [神经科学];
学科分类号:
071006 ;
摘要:
Fetal Alcohol Spectrum Disorder (FASD) comprises a group of neurodevelopmental deficits caused by alcohol exposure during pregnancy. Clinical studies suggest that while the male progeny experiences serious neurodevelopmental defects, female patients have more severe cognitive, social, and affective symptoms. Other than sex, dose, frequency, and timing of exposure determine the neurobehavioral outcomes in young and adult progeny. In this regard, human studies indicate that some individuals relapse during late-term gestational periods. In mice, this interval corresponds to the first 10 days after birth (postnatal, P0-P10). In our model of postnatal ethanol exposure (PEEP0-P10), we tested whether adult female and male offspring show deficits in sociability, anxiety-like, reward consumption, and action-outcome associations. We report that female PEEP0-P10 offspring have mild social impairments and altered extinction of operant responding in the absence of anxiety-like traits and reward consumption defects. None of these deficits were detected in the male PEEP0-P10 offspring. Our data provide novel information on sex-specific neurobehavioral outcomes of postnatal ethanol exposure in female adult offspring.
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页数:13
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