Acute hypoxia causes hyperventilation, sighs and arousal from sleep. The role of C1 neurons in mediating hypoxia counter-regulation in a behaving animal remains untested. We determined sufficiency by optogenetic methods. Channelrhodopsin-2 was selectively introduced into C1 neurons of Tyrosine Hydroxylase Cre-driver rats (Cre/0) with a Cre-dependant adeno-associated viral vector (AAV2 DIO-EF1alpha-ChR2-EYFP). Sleep stages were identified from EEG and neck EMG recordings. Breathing was measured using whole body plethysmography and blood pressure by telemetry. During non-rapid eye movement sleep (nREM), unilateral photostimulation of C1 neurons produced arousal in 84 ± 4% of trials and sighs in 68 ± 7% of trials and increased respiratory frequency by 26 ± 5 bpm (n=5). During quiet awake states, C1 stimulation also caused sighs and increased breathing rate. This increase in breathing by C1 stimulation was occluded by hypoxia (12% O2), but not hypercapnia (6% CO2), despite the significantly higher basal ventilation under hypercapnia. This evidence suggests that the C1 neurons that activate breathing are themselves activated by hypoxia and drive the ventilatory response and arousal from sleep.
|Number of pages||1|
|Issue number||1 supplement|
|Publication status||Published - Apr 2014|