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. Author manuscript; available in PMC: 2017 Sep 13.
Published in final edited form as: Nat Neurosci. 2017 Mar 13;20(5):700–707. doi: 10.1038/nn.4526

Figure 5. Corticosterone is released by C1 stimulation and restraint stress but plays no detectable role in protecting kidneys from renal ischemia-reperfusion injury (IRI).

Figure 5

(a) Restraint stress increased plasma corticosterone in DBH-cre mice. Statistics: unpaired t test; [t(10) = 4.991, P = 0.0005]. *** P < 0.001 vs. Restraint(−). (b) C1 neuron optogenetic stimulation (AAV2–DIO–EF1α–ChR2–mCherry, ChR2) increased plasma corticosterone in DBH-cre mice whereas laser light alone was ineffective in DBH-cre mice injected with control vector (AAV2–DIO–EF1α–mCherry, mCherry). Laser: laser stimulation (5 Hz for 10 min). Statistics: one-way ANOVA with Tukey–Kramer test; [F(2, 21) = 6.959, P = 0.0048]. * P < 0.05 vs. ChR2:Laser(−) and mCherry:Laser(+). (c) Mifepristone (30 mg/kg) did not alter the protective effect of C1 neuron stimulation against renal IRI in DBH-cre mice (n = 6/group). Statistics: unpaired t test; t(10) = 0.495, P = 0.6313).

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