Figure 2.

Spinal aPKC activity following a neural apnea stabilizes, but does not maintain iPMF. A. Representative compressed and integrated phrenic neurograms before, during and for 90 min following a 30 min neural apnea, illustrating that a control injection of intrathecal scrPKCζ-PS 10 min (scrPKCζ-PS-10; top) following resumption of respiratory neural activity did not impair neural apnea-induced iPMF. By contrast, intrathecal PKCζ-PS delivered 10 min (PKCζ-PS-10; middle), but not 45 min (PKCζ-PS-45; bottom), following resumption of respiratory neural activity returned phrenic burst amplitude toward baseline. Arrows indicate time points of drug delivery. B. Average change in phrenic burst amplitude from baseline for 90 min following neural apnea in rats receiving intrathecal scrPKCζ-PS-10 (triangles), PKCζ-PS-10 (circles) or PKCζ-PS-45 (gray square) at time points after resuming respiratory neural activity. Arrows indicate time points of drug delivery (black arrow for scrPKCζ-PS-10 and PKCζ-PS-10; gray arrow for PKCζ-PS-45). All rats expressed significant increases in phrenic burst amplitude relative to baseline or time controls (not shown) immediately prior to drug injections, indicating iPMF. Significant iPMF was observed in rats receiving intrathecal scrPKCζ-PS-10 for up to 90 min (vs. baseline or time controls), whereas iPMF progressively declined following PKCζ-PS-10 injections, such that by 30 min following resumption of respiratory neural activity, iPMF was significantly decreased from the pre-PKCζ-PS-10 injection value. No impairment in iPMF was observed in PKCζ-PS-45 rats. Intrathecal PKCζ-PS-10 was significantly lower than scrPKCζ-PS-10 and PKCζ-PS-45 at 60 and 90 min following neural apnea. Mean values + SEM. Filled symbols indicate significantly different than baseline. *significantly different from pre-injection time point. # significantly different from PKCζ-PS-10 rats. p<0.05