In anesthetized rats, unilateral retrotrapezoid nucleus (RTN) lesions markedly decreased baseline phrenic activity and the response to CO2 (E. E. Nattie and A. Li. Respir. Physiol. 97:63-77, 1994). Here we evaluate the effects of such lesions on resting breathing and on the response to hypercapnia and hypoxia in unanesthetized awake rats. We made unilateral injections [24 +/- 7 (SE) nl] of ibotenic acid (IA; 50 mM), an excitatory amino acid neurotoxin, in the RTN region (n = 7) located by stereotaxic coordinates and by field potentials induced by facial nerve stimulation. Controls (n = 6) received RTN injections (80 +/- 30 nl) of mock cerebrospinal fluid. A second control consisted of four animals with IA injections (24 +/- 12 nl) outside the RTN region. Injected fluorescent beads allowed anatomic identification of lesion location. Using whole body plethysmography, we measured ventilation in the awake state during room air, 7% CO2 in air, and 10% O2 breathing before and for 3 wk after the RTN injections. There was no statistically significant effect of the IA injections on resting room air breathing in the lesion group compared with the control groups. We observed no apnea. The response to 7% CO2 in the lesion group compared with the control groups was significantly decreased, by 39% on average, for the final portion of the 3-wk study period. There was no lesion effect on the ventilatory response to 10% O2. In this unanesthetized model, other areas suppressed by anesthesia, e.g., the reticular activating system, hypothalamus, and perhaps the contralateral RTN, may provide tonic input to the respiratory centers that counters the loss of RTN activity.

Objective: To determine if apneic preterm infants currently treated with methylxanthines develop evidence of sleep deprivation from cumulative arousal and motor activational effects.Study Design: Sleep, wake, arousal and actigraphic movements were monitored in extubated clinically stable premature infants (N ¼ 37). Neonates were free of other medications for >72 h and were grouped based on methylxanthine exposure: >5 days with caffeine (n ¼ 14), >5 days theophylline (n ¼ 13) or no prior exposure (n ¼ 10).Result: Duration of methylxanthine treatment predicted increased arousals, wakefulness and actigraphic movements, and decreased active sleep. Recording from 1200 to 0500 hours, methylxanthine-treated groups showed reductions in all arousal parameters: waking state, number of wake epochs, brief arousals and composite arousal index, and shorter fast-burst, sleep-related motility than untreated controls. Conclusion:In apneic preterms, chronic methylxanthine treatment appears to produce sleep deprivation secondary to the stimulatory action of methylxanthines on arousal and motor systems.

Low risk, premature infants between 30 to 35 weeks post-conceptual age (PCA) residing in an neonatal intensive care unit environment were observed in the home incubator for spontaneous yawning from 2400 to 0500 hr. Videorecordings were analyzed for the behavioral states of quiet sleep (QS), active sleep (AS), wake (W), and drowse (D) in 3-min epochs as well as the contextual behaviors before and after yawn events using a 1-min window. Yawning periods predicted higher levels of motoric activation than nonyawn periods. Sequence analysis of preceding and following states with or without yawns were examined for stability or change. All states with or without yawn events had state stability for the preceding and following epochs, with two exceptions: 1) D state with yawning was associated with state change in the preceding 3-min epoch (most often W), and 2) D state without yawning was associated with state change in the following epoch (W or AS). Yawns were not present in QS. The results suggest that yawning is associated with increased behavioral arousal that is not state-specific. However, yawning in D state predicts state transitions in the preceding, but not the following, epoch. It is proposed that D may be an unstable state that becomes more stable when yawning is present.

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