NDLI: Dihydromyricetin Prevents Fetal Alcohol Exposure-Induced Behavioral and Physiological Deficits: The Roles of GABA$

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Dihydromyricetin Prevents Fetal Alcohol Exposure-Induced Behavioral and Physiological Deficits: The Roles of GABA$_{A}$ Receptors in Adolescence

Content Provider	Springer Nature Link
Author	Liang, Jing Shen, Yi Shao, Xuesi M. Scott, Michael B. Ly, Eddie Wong, Stephanie Nguyen, Albert Tan, Kevin Kwon, Bill Olsen, Richard W. Spigelman, Igor
Copyright Year	2014
Abstract	Fetal alcohol exposure (FAE) can lead to a variety of behavioral and physiological disturbances later in life. Understanding how alcohol (ethanol, EtOH) affects fetal brain development is essential to guide the development of better therapeutics for FAE. One of EtOH’s many pharmacological targets is the γ-aminobutyric acid type A receptor (GABA$_{A}$R), which plays a prominent role in early brain development. Acute EtOH potentiates inhibitory currents carried by certain GABA$_{A}$R subtypes, whereas chronic EtOH leads to persistent alterations in GABA$_{A}$R subunit composition, localization and function. We recently introduced a flavonoid compound, dihydromyricetin (DHM), which selectively antagonizes EtOH’s intoxicating effects in vivo and in vitro at enhancing GABA$_{A}$R function as a candidate for alcohol abuse pharmacotherapy. Here, we studied the effect of FAE on physiology, behavior and GABA$_{A}$R function of early adolescent rats and tested the utility of DHM as a preventative treatment for FAE-induced disturbances. Gavage administration of EtOH (1.5, 2.5, or 5.0 g/kg) to rat dams on day 5, 8, 10, 12, and 15 of pregnancy dose-dependently reduced female/male offspring ratios (largely through decreased numbers of female offspring) and offspring body weights. FAE (2.5 g/kg) rats tested on postnatal days (P) 25–32 also exhibited increased anxiety and reduced pentylenetetrazol (PTZ)-induced seizure threshold. Patch-clamp recordings from dentate gyrus granule cells (DGCs) in hippocampal slices from FAE (2.5 g/kg) rats at P25-35 revealed reduced sensitivity of GABAergic miniature inhibitory postsynaptic currents (mIPSCs) and tonic current (I$_{tonic}$) to potentiation by zolpidem (0.3 μM). Interestingly, potentiation of mIPSCs by gaboxadol increased, while potentiation of I$_{tonic}$ decreased in DGCs from FAE rats. Co-administration of EtOH (1.5 or 2.5 g/kg) with DHM (1.0 mg/kg) in pregnant dams prevented all of the behavioral, physiological, and pharmacological alterations observed in FAE offspring. DHM administration alone in pregnant rats had no adverse effect on litter size, progeny weight, anxiety level, PTZ seizure threshold, or DGC GABA$_{A}$R function. Our results indicate that FAE induces long-lasting alterations in physiology, behavior, and hippocampal GABA$_{A}$R function and that these deficits are prevented by DHM co-treatment of EtOH-exposed dams. The absence of adverse side effects and the ability of DHM to prevent FAE consequences suggest that DHM is an attractive candidate for development as a treatment for prevention of fetal alcohol spectrum disorders.
Starting Page	1147
Ending Page	1161
Page Count	15
File Format	PDF
ISSN	03643190
Journal	Neurochemical Research
Volume Number	39
Issue Number	6
e-ISSN	15736903
Language	English
Publisher	Springer US
Publisher Date	2014-03-28
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Fetal alcohol spectrum disorders Pregnancy Brain development Anxiety Seizure Tolerance Ethanol Zolpidem Gaboxadol Dihydromyricetin Neurosciences Neurochemistry Biochemistry Cell Biology Neurology
Content Type	Text
Resource Type	Article
Subject	Medicine Biochemistry Cellular and Molecular Neuroscience

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Dihydromyricetin Prevents Fetal Alcohol Exposure-Induced Behavioral and Physiological Deficits: The Roles of GABA$_{A}$ Receptors in Adolescence