Behavior of hypoglossal inspiratory premotor neurons during the carbachol-induced, REM sleep-like suppression of upper airway motoneurons

In individuals with compromised upper airway anatomy, genioglossus (GG), th e main protruder muscle of the tongue, is an important upper airway dilator which helps prevent upper airway obstructions. During rapid eye movement ( REM) sleep, both the tonic and inspiratory-modulated components of GG activ ity are suppressed in parallel with the characteristic postural atonia. We tested whether the REM sleep-related reduction in the respiratory activity of GG may, in part, result from a reduced inspiratory drive relayed to hypo glossal (XII) motoneurons from their premotor medullary inspiratory neurons . In 15 urethane-anesthetized, paralyzed, vagotomized and artificially vent ilated rats, we recorded XII nerve activity and the extracellular activity of medullary inspiratory-modulated neurons antidromically activated with la tencies of 0.8 ms+/-0.3(SD) from within (n=19) or adjacent to (n=11) the XI I nucleus. Carbachol (10-20 nl. 10 mM), a cholinergic agonist, was microinj ected into the dorsomedial pens. Such injections trigger a REM sleep-like s tate in chronically instrumented. intact animals and, in anesthetized rats, produce respiratory and electrocortical changes similar to those of REM sl eep. Following the injections, the respiratory component of XII nerve activ ity was depressed by 51+/-22%, while the mean inspiratory firing rate of th e neurons decreased by only 7.4+/-13.8% (from 69+/-34 Hz to 65+/-37 Hz; P<0 .02; n=30). The activity of ventral respiratory group (VRG) and reticular f ormation inspiratory neurons with axons within the XII nucleus was reduced by 10+/-14% (P<0.005; n=19), whereas the activity of neurons located near t he VRG that had axons passing below the XII nucleus did not change (n=5). T hus, the depressant effect of carbachol on medullary inspiratory neurons wa s slightly more pronounced in reticular formation was and VRG cells premoto r to XII motoneurons than in other medullary inspiratory cells. For all cel ls, the magnitude of the decrease of cell activity was not related to the m agnitude of depression of XII nerve activity, the simultaneously occurring decrease in respiratory rate or the cell's control firing rate. Since the m agnitude of this depressant effect on all cell types was disproportionately small when compared with the depression of XII nerve activity, the REM sle ep-like decrease in GG activity must be mainly mediated by non-respiratory premotor pathways.