Do neurotoxic lesions in rostral medullary nuclei induce/accentuate hypoventilation during NREM sleep?

Experimentally induced neuronal dysfunction in respiratory regions of the rostral medulla decrease breathing more in anesthetized mammals than in awake mammals. Sleep is similar to anesthesia in that excitatory inputs to respiratory neurons are reduced compared to the awake state; thus, we hypothesized that neurotoxic lesions in rostral medullary nuclei would, relative to wakefulness (WK), induce and/or accentuate hypoventilation during non-rapid eye movement (NREM) sleep. To test the hypothesis, goats were studied between 21:00 h and 03:00 h: (1) before and 30 days after chronically implanting microtubules bilaterally into the rostral medulla and, (2) 9-15 h and 2-17 days after unilateral injections of 100 nl to 1 microl, 50 mM ibotenic acid into the vestibular, gigantocellularis reticularis, or facial nuclei, or the retrotrapezoid nucleus/parapyramidal region. Arterial blood was repeatedly sampled in all studies during WK, and NREM and rapid eye movement (REM) sleep states. There was no significant (P>0.10) change in Pa(CO(2)) between WK and NREM sleep (and REM sleep when sufficient data were obtained) before or after implantation of microtubules and in studies after creating the neurotoxic lesions. Breathing frequency also did not significantly (P>0.10) differ between states in any of the studies. The data thus did not support the hypothesis. We speculate that in goats efficient compensatory mechanisms maintain Pa(CO(2)) homeostasis during normal sleep and the same and/or other mechanisms maintain homeostasis when excitatory drive is further reduced by lesions in rostral medullary nuclei.