Abstract
Alcohol (ethanol) disturbs cognitive functions including learning and memory in humans, non-human primates, and laboratory animals such as rodents. As studied in animals, cellular mechanisms for learning and memory include bidirectional synaptic plasticity, long-term potentiation (LTP), and long-term depression (LTD), primarily in the hippocampus. Most of the research in the field of alcohol has analyzed the effects of ethanol on LTP; however, with recent advances in the understanding of the physiological role of LTD in learning and memory, some authors have examined the effects of ethanol exposure on this particular signal. In the present review, I will focus on hippocampal LTD recorded in rodents and the effects of fetal alcohol exposure on this signal. A synthesis of the findings indicates that prenatal ethanol exposure disturbs LTD concurrently with LTP in offspring and that both glutamatergic and γ-aminobutyric acid (GABA) neurotransmissions are altered and contribute to LTD disturbances. Although the ultimate mode of action of ethanol on these two transmitter systems is not yet clear, novel suggestions have recently appeared in the literature.
Highlights
Alcohol in beverages is the chemical molecule ethanol, which can be considered a “dirty drug”since it has no specific molecular target on cell membrane to induce its effects on organisms
The present chapter addresses the effects of ethanol on synaptic plasticity in the hippocampus after early-life ethanol exposure during pregnancy (i.e., prenatal ethanol exposure (PEE))
Given the role of activity-regulated cytoskeletal (ARC) in regulating synaptosomal AMPA-Rs, these results suggest a reduction in activity-dependent changes in AMPA-Rs in a way that diminishes the involvement of AMPA-Rs in dentate gyrus (DG) synaptic plasticity
Summary
Alcohol in beverages is the chemical molecule ethanol, which can be considered a “dirty drug”. Ethanol is pharmacologically classified as a psychoactive substance with a main depressive action on the CNS It has rewarding effects via its action through the brain reward circuit, which may explain the development of alcohol dependence. Brain Sci. 2017, 7, 157 consumption during pregnancy is gaining momentum as an issue because many studies indicate that low to moderate ethanol exposure during pregnancy may produce enduring deficits in the adult including learning and memory dysfunction. In this context, it is important to better understand the effects of prenatal alcohol exposure on cellular mechanisms of learning and memory. The present chapter addresses the effects of ethanol on synaptic plasticity in the hippocampus after early-life ethanol exposure during pregnancy (i.e., prenatal ethanol exposure (PEE))
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