Prenatal Ethanol (EtOH) Exposure Alters the Sensitivity of the Adult Dentate Gyrus to Acute EtOH Exposure

被引:6
作者
Helfer, Jennifer L. [1 ,2 ]
White, Emily R. [1 ,3 ]
Christie, Brian R. [1 ,2 ,3 ,4 ,5 ,6 ]
机构
[1] Univ Victoria, Div Med Sci, Victoria, BC V8P 5C2, Canada
[2] Univ Victoria, Dept Biol, Victoria, BC V8P 5C2, Canada
[3] Univ Victoria, Grad Program Neurosci, Victoria, BC V8P 5C2, Canada
[4] Univ British Columbia, Grad Program Neurosci, Vancouver, BC V5Z 1M9, Canada
[5] Univ British Columbia, Dept Cellular & Physiol Sci, Vancouver, BC V5Z 1M9, Canada
[6] Univ British Columbia, Brain Res Ctr, Vancouver, BC V5Z 1M9, Canada
关键词
Acute Ethanol; Fetal Alcohol Spectrum Disorders; Hippocampal Formation; Synaptic Plasticity; Long-Term Potentiation; LONG-TERM POTENTIATION; NMDA RECEPTOR SUBUNITS; FETAL ALCOHOL EXPOSURE; GABA(A) RECEPTORS; RATS; CA1; UNDERNUTRITION; HIPPOCAMPUS; MODULATION; INHIBITION;
D O I
10.1111/acer.12227
中图分类号
R194 [卫生标准、卫生检查、医药管理];
学科分类号
摘要
BackgroundPrenatal ethanol (EtOH) exposure results in a spectrum of structural, cognitive, and behavioral abnormalities, collectively termed fetal alcohol spectrum disorders (FASDs). The hippocampal formation, an area of the brain strongly linked with learning and memory, is particularly vulnerable to the teratogenic effects of EtOH. Prenatal EtOH exposure can lead to long-lasting impairments in the ability to process spatial information, as well as produce long-lasting deficits in the ability of animals to exhibit long-term potentiation (LTP), a biological model of learning and memory processing. These deficits also have the ability to facilitate EtOH and/or other drug abuse later in life. This study sought to determine prenatal EtOH exposure altered the effects of acute EtOH application on synaptic plasticity. MethodsPrenatal EtOH exposure was modeled using a liquid diet where dams were given 1 of 3 diets: (i) a liquid diet containing EtOH (35.5% EtOH-derived calories), (ii) a liquid diet, isocaloric to the EtOH diet, but with maltose-dextrin substituting for the EtOH-derived calories, and (iii) an ad libitum diet of standard rat chow. Extracellular recordings from transverse brain slices (350m) prepared from 50- to 70-day-old rats, following prenatal EtOH exposure (gestational day 1 to 21). LTP was examined in the dentate gyrus following acute EtOH exposure (0, 20, or 50mM) in these slices. ResultsPrenatal EtOH exposure attenuated LTP in the adult dentate gyrus. In control offspring, acute application of EtOH in adulthood attenuated (20mM) or blocked (50mM) LTP. Conversely, the effect of acute EtOH application on LTP was not as pronounced in prenatal EtOH offspring. ConclusionsPrenatal EtOH exposure alters the sensitivity of the adult dentate gyrus to acute EtOH application producing a long-lasting tolerance to the inhibitory effects of EtOH. This decreased sensitivity may provide a mechanism promoting the formation of drug-associated memories and help explain the increased likelihood of developing an alcohol dependency often observed in individuals with FASDs.
引用
收藏
页码:135 / 143
页数:9
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