Abstract
It has been previously shown that 40% of murine cortical interneurons are eliminated via apoptosis during the first two weeks of postnatal development [1], [2], [3]. Here, we report data on the effect of ethanol exposure on this process in a mouse model of binge-like alcohol exposure during last trimester of human pregnancy (equivalent to the first postnatal week in mice). We used transgenic mice that express the Venus fluorescent protein in GABAergic interneurons under the control of the vesicular GABA transporter promoter (VGAT-Venus mice) [4]. Mice were exposed to air (controls) or ethanol for 4 hr/day on postnatal days 4 to 9 using vapor inhalation chambers [5]. This exposure paradigm produces peak blood ethanol concentrations between 300 and 400 mg/dl. Transcardial perfusions were performed under anesthesia at postnatal days 5, 7, 10 and 30. Cryostat-prepared floating sections were stained with the fluorescent DNA dye, 4'6-diamidino-2-phenylindole (DAPI). We then quantified the density of Venus-positive GABAergic interneurons in layers I, II-IV and V of the retrosplenial cortex, which is part of the limbic memory system [6], and is sensitive to ethanol-induced apoptosis during the first postnatal week in mice [7], [8], [9], [10], [11]. The data show that density of interneurons decreases in the retrosplenial cortex layers during the first week of life and that ethanol exposure does not significantly alter this process. These data may be of interest to investigators who are studying the effect of ethanol and other teratogenic agents on developing interneurons in the cerebral cortex.