Editorial
Copyright ©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Neurol. Mar 28, 2017; 7(1): 1-5
Published online Mar 28, 2017. doi: 10.5316/wjn.v7.i1.1
Drinking during pregnancy: Potential role of endocannabinoid signaling in fetal alcohol effects
Basalingappa L Hungund
Basalingappa L Hungund, Nathan Kline Institute for Psychiatric Research, Orangeburg, NY 10962, United States
Basalingappa L Hungund, New York State Psychiatric Institute, New York, NY 10032, United States
Basalingappa L Hungund, Department of Psychiatry, College of Physicians and Surgeons, Columbia University, New York, NY 10032, United States
Author contributions: All the authors contributed to the manuscript.
Conflict-of-interest statement: The authors declare no conflicts of interest regarding this manuscript.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Basalingappa L Hungund, PhD, Nathan Kline Institute for Psychiatric Research, 140 Old Orangeburg Rd, Orangeburg, NY 10962, United States. hungund@nki.rfmh.org
Telephone: +1-845-3985442 Fax: +1-845-3985451
Received: August 30, 2016
Peer-review started: September 1, 2016
First decision: October 26, 2016
Revised: November 12, 2016
Accepted: December 16, 2016
Article in press: December 19, 2016
Published online: March 28, 2017
Processing time: 205 Days and 23.7 Hours
Abstract

Alcohol is a well-recognized teratogen that can cause variable physical and behavioral effects on the fetus. Alcohol use and abuse during pregnancy is one of the major health and societal problems and has been linked to a wide range of birth defects in the offspring collectively termed as fetal alcohol spectrum disorder (FASD). The severity of abnormalities may depend on a number of factors that include the amount, the frequency, the period during gestation and the route of alcohol administration. The current knowledge about the neurobiological basis of FASD is limited. However, recent studies have suggested that the membrane-derived lipids especially bioactive endogenous cannabinoids (eCB) such as arachidonyl ethanolamide and 2-arachidonyl glycerol resulting from alcohol exposure, may play a significant role in modulating neurophysiological and neurobehavioral effects in chronic alcohol exposed adult animals. Based on these findings and on reported studies on the role of eCB signaling in neurodevelopment and behavior, it is speculated that the eCB signaling may play a critical role in fetal alcohol syndrome and FASD-related behavioral effects. The current discussion will touch upon some of the mechanistic explanations about the role of eCB signaling system in FASD and provide further guidance for future direction.

Keywords: Lipid; Cannabinoids 1 receptor; Alcohol; γ-aminobutyric acid; Endocannabinoid; Fetal alcohol spectrum disorder

Core tip: Drinking during pregnancy leads to severe neurobiological consequences in the fetus and results in a variety of morphological and neurobehavioral abnormalities including mental retardation. One of the promising neurobiological mechanisms that can explain fetal alcohol spectrum disorder as discussed in this editorial is that of the possible role of alcohol-induced alteration in the levels of bioactive endogenous cannabinoids (eCBs) that are derived from membrane lipids and eCB signaling. Further studies exploring dietary supplementation with unsaturated fatty acids that can regulate the levels of the eCBs and testing of the drugs targeted against the eCB signaling, may have significant therapeutic value.