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

Fig. 1.

Fig. 1.

A–D: representative traces of compressed integrated phrenic neurograms. BDNF-induced pMF is MEK/ERK independent since intrathecal delivery of the MEK/ERK inhibitor U0126 does not affect pMF. A: intrathecal MEK/ERK inhibitor U0126 (100 μM, 12 μl) administration 20 min before intrathecal BDNF administration had no significant effect on pMF. B: intrathecal BDNF after the inhibitor vehicle (20% DMSO-80% saline) elicits pMF. C: MEK/ERK 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 (BL). MEK/ERK inhibitor + BDNF (n = 6), Inhibitor Vehicle + BDNF (n = 10), MEK/ERK inhibitor + aCSF (n = 6), and Time Control (n = 8) groups were compared to determine significance between groups. There were no significant differences at any time between MEK/ERK inhibitor + BDNF- vs. inhibitor vehicle + BDNF-treated rats. There were no significant differences at any time between MEK/ERK inhibitor + aCSF and Inhibitor Vehicle + aCSF groups. There were significant differences between the MEK/ERK inhibitor + BDNF and Inhibitor Vehicle + BDNF groups vs. MEK/ERK inhibitor + aCSF and Time Control groups at 60 and 90 min after BDNF or vehicle injection. Significance is P ≤ 0.05: #significantly different from MEK/ERK inhibitor + aCSF; @significantly different from Inhibitor Vehicle + aCSF. F: group data for phrenic frequency; there were no significant differences in frequency between any groups at any time.