75 = 0 3, P = 0 86, Fig  1C)

Overall, JS animals had hig

75 = 0.3, P = 0.86, Fig. 1C).

Overall, JS animals had higher expression of hippocampal MR mRNA than controls (F1,2.81 = 25.13, P = 0.02, Fig. 4A) and lower GR:MR ratio (F1,2.58 = 22.78, P = 0.02, data box-cox transformed, Fig. 4B) than control animals. There was no interaction between group and sex on hippocampal MR expression (F1,16.3 = 0.01, Inhibitors,research,lifescience,medical P = 0.91) or GR:MR ratio (data box-cox transformed, F1,16.15 = 0.003, P = 0.95). There was no difference between control and JS animals in hippocampal GR expression (F1,9.48 = 0.23, P = 0.64) and no group × sex interaction (F1,19.94 = 0.26, P = 0.62). Figure 4 Hippocampal mRNA expression. (A) MR and (B) GR:MR ratio in control (Con) and juvenile Stress (JS) animals. Hippocampal mRNA expression of (C) GR, (D) GR:MR ratio in males and females. Error bars represent Inhibitors,research,lifescience,medical 1 SE, bars connected by an asterisk are … Females expressed greater hippocampal mRNA levels of GR (F1,19.94 = 5.88, P = 0.02, Fig. 4C) and a higher GR:MR ratio (F1,16.15 = 7.04, P = 0.02, data box-cox transformed, Fig. 4D) than males. There were no sex differences in hippocampal

MR expression (F1,16.3 = 2.9, P = 0.1). There were no differences in the expression of the housekeeping gene, HPRT1, between groups (F1,8.59 = 1.33, P = 0.28), sexes (F1,14.38 = 0.17, P = 0.69), or group × sex interaction (F1,14.38 = 0.48, P = 0.5). Discussion Juvenile stress Inhibitors,research,lifescience,medical The experience of stress in the juvenile phase increased anxiety-like behavior on the Inhibitors,research,lifescience,medical EPM in adulthood. This result is in agreement with previous studies in rats, (Avital and Richter-Levin 2005; Tsoory et al. 2007; Ilin and Richter-Levin 2009), suggesting that

the effects of JS on anxiety are conserved across rats and mice. However, it contrasts with results from one study using mice, in which no effects of JS were found on adulthood behavior Inhibitors,research,lifescience,medical in an EPM (Peleg-Raibstein and Feldon 2011). One possible explanation for the disagreement between studies is differences in the type and duration of JS protocols used, as well as sample sizes. In particular, the previous study used 5 days of variable stress (including exposure to a shaking platform, water deprivation, and exposure to a predator, stressors not used in the present study) whereas 3 days were used in this study. Furthermore, sample sizes were significantly tuclazepam smaller (n = 7/group) in the Peleg-Raibstein and Feldon (2011) study, whereas the present study used 18 control and 17 stressed animals (combined over males and females). Our result also reflects the findings in human populations, in which juvenile or childhood stress shows a strong correlation with anxiety disorders in adulthood (Green et al. 2010). The see more specific mechanisms underlying these disruptions are not well understood, although existing studies suggest that reprogramming of the HPA axis may be involved (Meaney et al. 2007; McGowan et al. 2009; Belay et al.

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