Acute intermittent hypoxia enhances nucleus of the solitary tract neuronal activity and requires NMDARs and CaMKII for phrenic long-term facilitation

Exposure to acute intermittent hypoxia (AIH) induced sustained increases in phrenic nerve activity (phrenic long-term facilitation, pLTF) that were associated with increased nucleus tractus solitarii (nTS) neuronal Ca 2+ and action potential discharge. nTS CaMKII activity was critical for pLTF development and AIH-induced increases in neuronal discharge. In contrast, nTS NMDA receptor (NMDAR) activation, but not CaMKII activity, was required for maintaining AIH-induced pLTF. Increased nTS neuronal activity, NMDAR activation, and CaMKII are critical for AIH-induced neuroplasticity in central cardiorespiratory output.