Abstract
Fetal alcohol spectrum disorder (FASD) is associated with learning and memory alterations that could be, in part, a consequence of hippocampal damage. The CA3 hippocampal subfield is one of the regions affected by ethanol (EtOH), including exposure during the third trimester-equivalent (i.e., neonatal period in rats). However, the mechanism of action of EtOH is poorly understood. In CA3 pyramidal neurons from neonatal rats, dendritic BDNF release causes long-term potentiation of the frequency of GABAA receptor-mediated spontaneous postsynaptic currents (LTP-GABAA) and this mechanism is thought to play a role in GABAergic synapse maturation. Here, we show that short- and long-term exposure of neonatal male rats to low EtOH concentrations abolishes LTP-GABAA by inhibiting L-type voltage-gated Ca2+ channels. These findings support the recommendation that even light drinking should be avoided during pregnancy.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Animals
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Animals, Newborn
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Brain-Derived Neurotrophic Factor / metabolism
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CA3 Region, Hippocampal / drug effects*
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CA3 Region, Hippocampal / growth & development
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CA3 Region, Hippocampal / physiology
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Calcium Channels, L-Type / metabolism
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Central Nervous System Depressants / administration & dosage
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Central Nervous System Depressants / pharmacology*
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Ethanol / administration & dosage
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Ethanol / pharmacology*
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In Vitro Techniques
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Long-Term Potentiation / drug effects*
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Long-Term Potentiation / physiology
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Male
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Pyramidal Cells / drug effects*
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Pyramidal Cells / growth & development
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Pyramidal Cells / physiology
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Rats
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Rats, Sprague-Dawley
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Receptors, GABA-A / metabolism
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Time Factors
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gamma-Aminobutyric Acid / metabolism
Substances
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Brain-Derived Neurotrophic Factor
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Calcium Channels, L-Type
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Central Nervous System Depressants
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Receptors, GABA-A
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Ethanol
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gamma-Aminobutyric Acid