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. 2014 Aug 7;117(7):682–693. doi: 10.1152/japplphysiol.00342.2014

Fig. 1.

Fig. 1.

Inactivity-induced phrenic motor facilitation (iPMF) and burst frequency facilitation are differentially regulated in Harlan Sprague-Dawley (HSD) and Charles River Sprague-Dawley (CRSD) rat substrains. A: representative compressed phrenic neurograms depicting baseline, 30 min of neural apnea, and for 60 min after the resumption of phrenic neural activity in HSD and CRSD rats receiving intrathecal vehicle. Black arrows denote intrathecal delivery of vehicle. B: average phrenic burst amplitude (% baseline) for 60 min post neural apnea or an equivalent duration in time controls (triangles) in HSD (circles) and CRSD (squares) rats pretreated with vehicle. HSD rats exposed to neural apnea expressed a significant increase in phrenic burst amplitude relative to time controls at all time points, indicating long-lasting iPMF. By contrast, CRSD rats exposed to neural apnea expressed a smaller but significant increase in phrenic burst amplitude relative to time controls at 5 and 15 min, which returned to baseline 30 min post neural apnea, suggesting transient iPMF. C: average phrenic burst frequency (Δ baseline) in HSD (circles) and CRSD (squares) rats pretreated with vehicle for 60 min post neural apnea or an equivalent duration in time controls (triangles). HSD rats exposed to neural apnea expressed a significant increase in phrenic burst frequency relative to time controls at all time points. CRSD rats exposed to neural apnea expressed a smaller but significant increase relative to time controls only at 5 min post neural apnea. Values are means ± SE. *Significantly different than time controls; #significantly different than CRSD rats; P < 0.05.