Ethanol Induces Fas/Apo [Apoptosis]‐1 mRNA and Cell Suicide in the Developing Cerebral Cortex

• DOI: 10.1111/j.1530-0277.2000.tb02022.x
• Publication Date: 2006-04-11T10:33:44Z
• Authors: Zulfiqar F. Cheema; James R. West; Rajesh C. Miranda
• Keywords: Propidium iodide

Animal studies modeling fetal alcohol syndrome have demonstrated that developmental exposure to is associated with decreased brain weight and significant neuronal loss in multiple regions of the developing brain. Our previous data suggest Fas/Apo [apoptosis]-1 receptor transiently expressed cerebral cortex during peak period naturally occurring apoptotic cell death maximum sensitivity alcohol. Therefore, we hypothesized ethanol increases expression suicide receptors such as Fas/Apo-1 leads an upregulation or extension normal apoptosis consequent disorganization neural circuitry.Ethanol was administered one four doses (120, 320, 630, 950 mg/dl) organotypic explant cultures established from postnatal day 2 rats maintained for 6 days vitro. The number cells expressing mRNA counted. Apoptosis measured by use two independent assays; a enzyme-linked immunosorbent assay DNA fragmentation flow cytometric analysis Annexin-V binding phosphatidylserine externalized outer leaflet plasma membrane. Necrosis also estimated measures, amount lactate dehydrogenase released into culture medium were positive both propidium iodide.A significantly larger cortical at lower (120 320 than higher (630 mg/dl). Furthermore, induced dose-related manner, observed dose 630 mg/dl case translocation Ethanol did not induce necrosis any ethanol.Our induces susceptibility signals low upregulating mRNAs cytotoxic cortex. However, itself specifically only doses.