['Patients with obstructive sleep apnea (OSA) adapt to the anatomical vulnerability of their upper airway by generating increased activity in upper airway-dilating muscles during wakefulness. Norepinephrine (NE) and serotonin (5-HT) mediate, through α₁-adrenergic and 5-HT₂A receptors, a wake-related excitatory drive to upper airway motoneurons. In patients with OSA, this drive is necessary to maintain their upper airway open. We tested whether chronic intermittent hypoxia (CIH), a major pathogenic factor of OSA, affects aminergic innervation of XII motoneurons that innervate tongue-protruding muscles in a manner that could alter their airway-dilatory action.', 'To determine the impact of CIH on neurochemical markers of NE and 5-HT innervation of the XII nucleus.', 'NE and 5-HT terminal varicosities and α₁-adrenergic and 5-HT₂A receptors were immunohistochemically visualized and quantified in the XII nucleus in adult rats exposed to CIH or room air exchanges for 10 h/d for 34 to 40 days.', 'CIH-exposed rats had approximately 40% higher density of NE terminals and approximately 20% higher density of 5-HT terminals in the ventromedial quadrant of the XII nucleus, the region that controls tongue protruder muscles, than sham-treated rats. XII motoneurons expressing α₁-adrenoceptors were also approximately 10% more numerous in CIH rats, whereas 5-HT₂A receptor density tended to be lower in CIH rats.'] Does chronic intermittent hypoxia alter density of aminergic terminals and receptors in the hypoglossal motor nucleus?