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. Author manuscript; available in PMC: 2017 Nov 1.
Published in final edited form as: Alcohol. 2017 Feb 20;60:135–147. doi: 10.1016/j.alcohol.2017.01.006

Fig. 4.

Fig. 4

Tbr2-im at the E17 frontal cortex across experimental groups. Structural abnormalities were observed during immunophenotypic investigation. Notably, the thickness of cortical plate (J) as well as the entire thickness of frontal cortex (I) were markedly reduced in Alcohol group frontal cortex as compared to their Chow and PF control cortices (A–C). Fetal alcohol exposure also increased the proportion of SVZ + VZ/entire cortical thickness (K) as compared to controls. Lateral Ventricle (LV) expansion was also observed in E17 alcohol cortices (A–C). (G) Finally, Tbr2-im (a marker for neural progenitor migration) was normally observed as a radially extending fiber ascending from the base of the lateral ventricle up to the pial surface. Alcohol noticeably reduced the Tbr2 immunoreactivity in the CP layer. E16 Chow brains were used as developmental stage controls and more closely resembled the E17 alcohol developmental state than E17 Chow (C–D, G–H). Quantitative measurements among the three groups were analyzed by one-way ANOVA, and the difference between paired groups were compared by Student t-test *p < 0.05, **p < 0.005. N (structural analysis) = Chow (5), PF (5), Alc (5). N (Tbr2-im analysis) = Chow (3), PF (3), Alc (3), E16 Chow (3). SVZ/VZ (Subventricular Zone/Ventricular Zone); IZ (Intermediate Zone); SP (Subplate); CP (Cortical plate).