FIGURE 4.

ECR1(C) activity is controlled by MEK/p38 kinase signaling in hypothalamic neurons. Primary rat hypothalamic neurons were cultured for 3 days and then transfected with a pECR1(C) construct and treated with angiotensin II (AngII, 10 μm) in the presence/absence of MEK kinase inhibitor (U0216, 1 μm) (A), JNK II inhibitor (SP600125, 50 nm) (B), or p38 kinase inhibitor (SB 202190, 10 μm) (C). The control is the pECR1(C) construct treated with a respective vehicle. Cells were incubated with treatment for 24 h and then assayed for luciferase activity. Cells were lysed, and a relative luciferase measurement was determined and normalized to an internal Renilla luciferase control (pRL-CMV). ns = not significant, *, p = ≤ 0.05, **, p = ≤ 0.01.