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Open AccessFeature PaperArticle

Postnatal Ethanol-Induced Neurodegeneration Involves CB1R-Mediated β-Catenin Degradation in Neonatal Mice

1
Division of Analytical Psychopharmacology, Nathan Kline Institute for Psychiatric Research, 140 Old Orangeburg Rd, Orangeburg, NY 10962, USA
2
New York State Psychiatric Institute, New York, NY 10032, USA
3
Department of Psychiatry, College of Physicians & Surgeons, Columbia University, New York, NY 10032, USA
4
Department of Psychiatry, New York University Langone Medical Center, New York, NY 10016, USA
*
Author to whom correspondence should be addressed.
Brain Sci. 2020, 10(5), 271; https://doi.org/10.3390/brainsci10050271
Received: 3 April 2020 / Revised: 21 April 2020 / Accepted: 26 April 2020 / Published: 1 May 2020
(This article belongs to the Special Issue Recent Advances in Fetal Alcohol Spectrum Disorder (FASD))
Alcohol consumption by pregnant women may produce neurological abnormalities that affect cognitive processes in children and are together defined as fetal alcohol spectrum disorders (FASDs). However, the molecular underpinnings are still poorly defined. In our earlier studies, we found that ethanol exposure of postnatal day 7 (P7) mice significantly induced widespread neurodegeneration mediated via endocannabinoids (eCBs)/cannabinoid receptor type 1 (CB1R). In the current study, we examined changes in the β-catenin protein levels that are involved in the regulation of neuronal function including neuronal death and survival. We found that moderate- and high-dose postnatal ethanol exposure (PEE) significantly reduced active-β-catenin (ABC) (non-phosphorylated form) protein levels in the hippocampus (HP) and neocortex (NC). In addition, we found that moderate- and high-dose PEE significantly increased the phosphorylated-β-catenin (p-β-catenin)/ABC ratios in the HP and NC. Antagonism/null mutation of CB1R before PEE to inhibit CC3 production mitigated the loss of ABC protein levels. Collectively, these findings demonstrated that the CB1R/β-catenin signaling mechanism causes neurodegeneration in neonatal mouse brains following PEE. View Full-Text
Keywords: alcohol; development; apoptosis; FASD; Wnt signaling alcohol; development; apoptosis; FASD; Wnt signaling
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MDPI and ACS Style

Subbanna, S.; Basavarajappa, B.S. Postnatal Ethanol-Induced Neurodegeneration Involves CB1R-Mediated β-Catenin Degradation in Neonatal Mice. Brain Sci. 2020, 10, 271.

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