The ischemic regulation of Cx36 by group II mGluRs is through cAMP/PKA-dependent signaling. A, B, Pharmacological treatments were performed in wild-type mouse mature neuronal cortical cultures that were subjected to sham OGD (A) or OGD (B) followed by assessment of Cx36 protein expression 2 h after sham OGD or OGD. Statistical data and representative blots are shown. Optical density signals are normalized relative to tubulin, and normalized values are compared with the control (set at 1.0; not shown in B). Statistical analysis was as follows: ANOVA with post hoc Tukey; statistical significance is shown relative to control (i), nontreated plus OGD (ii), LY379268 alone (iii), and LY341495 alone (iv); n = 7–11 per group; data are shown as mean ± SEM. Treatments were as follows: PKA(+), activation of the cAMP/PKA-dependent signaling by 8-Br-cAMP plus IBMX (100 μm plus 50 μm); PKA(−), blockade of the activity of PKA with KT5720 (0.5 μm); LY379268, 2 μm; LY341495, 2 μm; all agents were present in the culture medium for the time as described for Figure 2.