Skip to main content
. 2008 Feb 20;28(8):1854–1864. doi: 10.1523/JNEUROSCI.5110-07.2008

Figure 1.

Figure 1.

The mouse model of low-level chronic ethanol consumption used to examine the effect of in utero ethanol exposure on corticogenesis increases the size of embryos. A, B, Images of control (A1) and 2% ethanol-exposed (A2) embryos and brains (B) at E14.5. C, The body and brain weight were significantly increased with ethanol exposure (Student's t test; *p < 0.05) without altering the brain to body weight ratio (Student's t test; p = 0.96) as measured in the BAC-Lhx6 embryos (control, n = 8; ethanol, n = 9). Data are expressed as mean ± SEM. Asterisks denote a statistical difference compared with control. D, BAL was not significantly different between dams and embryos at time of killing within treatment groups (Student's t test; GAD67, n = 3, p = 0.86; BAC-Lhx6, n = 10, p = 0.44; GFP β-act, n = 7, p = 0.70) or between treatment groups (GAD67, 28.94 ± 1.97 mg/dl; BAC-Lhx6, 25.03 ± 1.59 mg/dl; GFP β-act, 24.95 ± 1.36 mg/dl; ANOVA, p = 0.42). Data are expressed as mean ± SEM. GAD67, GAD67-GFP transgenic mice; GFP β-act, GFP under the control of a β-actin/CMV promoter/enhancer sequence.