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. Author manuscript; available in PMC: 2012 Aug 1.
Published in final edited form as: Neurobiol Dis. 2011 Apr 20;43(2):356–363. doi: 10.1016/j.nbd.2011.04.004

Figure 3. 11β-Hydroxysteroid Dehydrogenase Type 2 (HSD2) inhibition alone produces GINA and is blocked by glucocorticoid receptor inhibition.

Figure 3

(A) The HSD2 inhibitor carbenoxolone (CARB; 100 mg/kg) dramatically potentiates EGL NPC apoptosis whether or not corticosterone is co-administered. (B) Photocomposite of activated caspase-3 immunoreactively reveals that, compared to saline (top), CARB treatment (bottom) dramatically increased the amount of activated caspase-3 positive NPCs (white arrows). Insets reflect magnified views of boxed regions with solid black lines defining the internal borders of each EGL and white dotted line defining the pial surface. Scale bars: 250 um. (C) The ability of the glucocorticoid receptor antagonist mifepristone to block CARB induced toxicity verifies that HSD2 mediates GINA. For all graphs the boxed numbers in each bar represents n per group. * p < 0.001, ** p < 0.01.