Figure 2.
Forebrain overexpression of 11β-HSD1 causes cognitive decline with aging. a, Left, Immunohistochemical localization of CamIIK-HSD1 transgene using HA-tag antibodies in cerebral cortex (A), hippocampus (B), amygdala (C), and lateral septum (D). Right, 11β-HSD1 activity (percentage conversion corticosterone-11-dehydrocorticosterone) was increased (*p < 0.05) in cerebral cortex and hippocampus of CamIIK-HSD1 (Tg) mice compared with wt, n = 7 per group. b, Aging (18 months), but not young (6–9 months) (n = 8/group), Tg mice display delayed learning of water maze task compared with age-matched wt littermates; *p < 0.05, compared with respective day 1 value. c, Attenuated retention of conditioned behavior in aging Tg mice. Young and aging Tg and wt mice were tested for latency to move from light to dark compartments on day 2 shock trial (D2.1) and 5 h postshock (D2.2); *p < 0.05 compared with D2.1 value.