Skip to main content
. 2017 Aug 30;118(5):2755–2762. doi: 10.1152/jn.00945.2016

Fig. 3.

Fig. 3.

A–D: representative traces of compressed integrated phrenic neurograms. BDNF-induced pMF is PKCθ dependent since the PKCθ inhibitor TIP abolishes pMF. A: intrathecal PKCθ inhibitor TIP (0.86 mM, 12 μl) administration 15 min before intrathecal BDNF abolishes pMF. B: intrathecal BDNF after the inhibitor vehicle elicits pMF. C: PKCθ inhibitor + BDNF vehicle (aCSF) does not exhibit pMF. D: intrathecal administration of inhibitor vehicle + aCSF does not exhibit pMF. E: group data for phrenic burst amplitude expressed as % change from baseline. PKCθ inhibitor + BDNF (n = 6), Inhibitor Vehicle + BDNF (n = 10), PKCθ inhibitor + aCSF (n = 5), and Time Control (n = 8) groups were compared to determine significance between groups. There were significant differences at 30, 60, and 90 min after BDNF between PKCθ inhibitor + BDNF and Inhibitor Vehicle + BDNF, PKCθ inhibitor + aCSF, and Inhibitor Vehicle + aCSF groups. There was no significant difference at any time between Inhibitor Vehicle + BDNF, PKCθ inhibitor + aCSF, and Inhibitor Vehicle + aCSF groups. Significance is P ≤ 0.05: #significantly different from PKCθ inhibitor + aCSF; @significantly different from Time Control; %significantly different from Inhibitor Vehicle + BDNF. F: group data for phrenic frequency; there were no significant differences in frequency between any groups at any time.