Aftereffects of 1-week chronic intermittent hypoxia on the jaw muscle electromyographic activities during sleep in young adult rats.

Obstructive sleep apnea (OSA) is associated with increased jaw muscle activity during sleep across a wide age range from childhood to adulthood. However, the contribution of intermittent hypoxia to jaw muscle activity remains unclear. We hypothesized that chronic intermittent hypoxia (CIH) enhances arousal-related jaw muscle activity during sleep through neuroplastic changes in trigeminal motor system in young adult rats. Six-week-old rats were exposed to CIH (nadir O_2, 5%) for 6 h/day during the light phase for 1 week. At 7 weeks of age, immunohistochemical analyses were performed to assess FosB expression in brainstem regions containing trigeminal premotor neurons and dopamine-β-hydroxylase-positive fiber density in the trigeminal motor nucleus. At 7 weeks of age after CIH exposure, electrophysiological recordings were conducted to analyze masseter and digastric muscle activity during sleep-wake cycles. CIH increased FosB expression in multiple brainstem regions containing trigeminal premotor neurons and enhanced noradrenergic fiber density in both dorsolateral and ventromedial regions of the trigeminal motor nucleus. Sleep architecture, electroencephalography spectral power, and open-field behavior remained unchanged between groups. While masseter muscle activity was stable across vigilance states, CIH selectively increased digastric muscle activity during arousal from sleep. One-week CIH induces plasticity in trigeminal circuits and enhances arousal-related jaw-opening muscle responsiveness in young adult rats, without altering overall sleep structure.