Fig. 7

PKR deficiency delayed hypothalamic CRH induction but did not affect the plasma corticosterone response. Hypothalamic CRH mRNA expression (a) and plasma corticosterone levels (b) were assessed at indicated times after E. coli challenge. As shown in a, genetic deletion of PKR abolished the elevation of CRH by E. coli at 4 h but triggered a delayed increase in the PKR−/− E. coli group at 48 h. n = 7–8 per group at 4 h, n = 6–8 per group at 48 h, and n = 9–11 per group at 120 h. *p < 0.05, **p < 0.01. In b, E. coli caused similar increases of plasma corticosterone at 4 h (16:00) in WT and PKR−/− mice. By 48 h (12:00), corticosterone levels in the E. coli-treated groups had returned to control levels. n = 7–10 per group at 4 h, n = 5–7 per group at 48 h; *p < 0.05, **p < 0.01