Figure 4. PKA and PKC antagonism in ipsilateral and contralateral PCtx in the presence of CRF. A, Quantification of the effect of BIS on CRFR1 activation in ipsilateral piriform cortical slices from brain-injured animals; *p < 0.05, n = 8 slices from eight rats/group. B, Quantification of the effect of the PKC inhibitor, PMA, on CRF-mediated activation of CRFR1 in ipsilateral piriform cortical slices from brain-injured animals; *p < 0.05, n = 9 slices from eight rats/group. C, Quantification of the effect of the PKA antagonist H89 on CRF-mediated activation of CRFR1 in ipsilateral piriform cortical slices from brain-injured animals; *p < 0.05, n = 9 slices from seven rats/group. D, Quantification of the effect of forskolin, an adenylate cyclase activator with or without subsequent administration of H89 on ipsilateral piriform cortical slices from brain-injured animals; *p < 0.05, n = 8 slices from six rats/group. E, Quantification of the effect of forskolin (an adenylyl cyclase activator) with or without subsequent administration of H89, on CRFR1 activation in contralateral piriform cortical slices from brain-injured animals; *p < 0.05, n = 7 slices from six rats/group. F, Quantification of the effect of the PKA inhibitor H89 on CRF-mediated activation of CRFR1 in contralateral piriform cortical slices from brain-injured animals; *p < 0.05, n = 6 slices from six rats/group. G, Quantification of the effect of the PKC antagonist BIS on CRF-mediated activation of CRFR1 in contralateral piriform cortical slices from brain-injured animals; *p < 0.05, n = 6 slices from six rats/group.