Prolonged reductions in respiratory neural activity in Harlan Sprague Dawley (HSD) rats elicit an atypical PKC (aPKC) dependent form of spinal plasticity called inactivity‐induced phrenic motor facilitation (iPMF), a rebound increase in phrenic burst amplitude that is apparent when respiratory neural activity is restored. In Charles River Sprague Dawley (CRSD) rats, iPMF is pattern sensitive and is only induced by intermittent, but not sustained neural apneas. We hypothesized that iPMF in CRSD requires spinal aPKC activity. Anesthetized and ventilated CRSD were hyperventilated to create five brief (~1 min) neural apneas, separated by 5 min. 10 min following intermittent neural apneas, rats received an aPKC inhibitor (ZIP) or scrambled ZIP in the intrathecal space over C4. As expected, significant iPMF was observed prior to intrathecal ZIP or scrambled ZIP (5 min post‐apnea: 56 + 8 and 57 + 12 %baseline; p<0.01). Subsequent intrathecal ZIP significantly attenuated iPMF (p<0.001), such that phrenic amplitude was no longer different from baseline at 60 min post‐intermittent apnea (6 + 7 %baseline; p>0.05). By contrast, rats receiving scrambled ZIP continued to express significant iPMF (69+8 %baseline; p<0.01). These data suggest that similar to iPMF following a prolonged apnea in HSD, increased phrenic burst amplitude following intermittent neural apnea in CRSD is dependent on spinal aPKC activity. NIH 105511