Exposure of anesthetized paralyzed vagotomized peripherally chemodener
vated cats to hypoxia results in initial depression and subsequent los
s of the phrenic neurogram. To determine whether hypoxic respiratory d
epression results from the inhibition of respiratory premotor neurons
by bulbospinal neurons of the Botzinger complex (Bot-E neurons), extra
cellular recordings were made of dorsal and ventral respiratory group
bulbospinal inspiratory neurons and Bot-E neurons during acute hypoxic
hypoxia. All neurons recorded decreased firing rate during hypoxia. B
ot-E neurons became silent before the loss of phasic phrenic activity
during hypoxia and commenced firing before or coincident with the retu
rn of the phrenic neurogram during reoxygenation. Inspiratory neurons
ceased firing coincident with phrenic silence. Dorsal respiratory grou
p and ventral respiratory group neurons that had a late onset of firin
g with respect to the phrenic neurogram during normoxia fired progress
ively earlier in inspiration during hypoxia, an effect that was revers
ed during reoxygenation. These data are consistent with inhibition and
/or disfacilitation as the mechanism of hypoxic respiratory depression
but suggest that Bot-E neurons are not the source of this inhibition.