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. 2021 May 26;41(21):4641–4657. doi: 10.1523/JNEUROSCI.0251-21.2021

Figure 10.

Figure 10.

Blockade of CRH1R(s) within the PVN abolishes the increased blood pressure evoked by the optogenetic stimulation of PVNAgtr1a. A, Schematic depicting the mouse line and experimental protocol. In this experiment, Agtr1a-Cre mice received a Cre-inducible AAV-ChR2-eYFP into the PVN. Following recovery, optogenetic stimulation (10 mW; 20 ms pulse width; 30 Hz; 1 min) of PVNAgtr1a was performed after PVN microinjections using a dual optical injector cannula. B, Representative pulsatile arterial blood pressure traces following blue laser stimulation (BLS) in PVNAgtr1a-ChR2, and BLS 5 min following the injection of vehicle (10% acetic acid, pH 7.4 – PVNAgtr1a-ChR2 (acetic acid)) or Astressin (200 μm; PVNAgtr1a-ChR2 (Astressin)) into the PVN. C, Grouped data demonstrating the change in SBP and mean arterial pressure (MAP). *p < 0.05; **p < 0.05; two-way ANOVA followed by Tukey's post for PVNAgtr1a-ChR2 (Astressin) versus PVNAgtr1a-ChR2. †p < 0.05; two-way ANOVA followed by Tukey's post for PVNAgtr1a-ChR2 (Astressin) versus PVNAgtr1a-ChR2 (acetic acid); n = 6 per group. Error bars indicate SEM.