Ethanol-Induced Apoptosis of Interneurons in the Neonatal GAD67-GFP Mouse Hippocampus

• 全文链接
• 请求原文

作   者：

Elena Ogievetsky;  Nailya Lotfullina;  Alina Minlebaeva;  Roustem Khazipov; 

作者机构：

Marseille 13273;  France;  INMED--INSERM U901;  163 avenue de Luminy; 

关键词：

Fetal alcohol syndrome;  Interneurons;  Neonate;  Alcoholism;  GABA;  Hippocampus; 

期刊名称：

BioNanoscience

i s s n：

2191-1630

年卷期：

2017 年 7 卷 1 期

页   码：

151-154

页   码：

摘   要：

Ethanol induces massive neuroapoptosis in the developing brain. However, whether ethanol-induced neuroapoptosis also involves GABA interneurons remains unknown. Here, we addressed this question in the postnatal days (P) P3-P24 GAD67-GFP mouse hippocampus using cleaved caspase-3 staining, a sensitive measure of ethanol-induced apoptotic neurodegeneration combined with DAPI staining to monitor the apoptotic nuclear degradation. We observed that 8 h following ethanol treatment (6 g/kg, intraperiotoneally), significant proportion of GAD67-GFP expressing hippocampal interneurons was stained with cleaved caspase-3 antibodies and displayed chromatin condensation with a formation of the DAPI-stained apoptotic bodies. Maximal number of the cleaved caspase-3 stained interneurons (16.6 % of the total number of GFP expressing neurons and 21.6 % of the total number of caspase-3 stained cells) was observed in the hippocampal slices from P6-9 mice, and minimal damage to interneurons was observed in P3-4 and>P11 mice. While the apoptotic interneurons were found in all hippocampal regions and layers, their highest density was observed in the CA1 region and hilus. Thus, ethanol-induced neuroapoptosis involves hippocampal interneurons that may contribute to the life-long neurobehavioral deficits, increased excitability, and higher incidence of seizures characteristic of the fetal alcohol spectrum disorders.