Figure 3.

Pharmacological reactivation of 3 mm K⁺ rhythms in preBötC slices after onset of in vitro apnea. A, In a m-preBötC[500/−0.70]W-P3 slice, the inspiratory rate slowed to 2 bursts/min after 185 min of recording, and rhythm stopped 3 min later. Such in vitro apnea was reversed by bath application of 6 mm K⁺ solution or the more specific respiratory stimulants TRH and rolipram. B, In a m-preBötC[500/−0.75]W-P2 slice, rhythm stopped 6 min after burst rate had dropped to 4 bursts/min after 2 h of recording. Eupneic bursts were activated by either 6 mm K⁺ or TRH, whereas SP induced bursting with a eupnea–sigh pattern. C, Burst rates of pharmacologically restored inspiratory rhythms in different preBötC slice types. After the onset of in vitro apnea, bursting was reactivated by 6 mm K⁺, TRH, SP, the NK1 receptor agonist GR73632, and rolipram in the slice types shown in the dashed box. Bars show means ± SEM; digits in bars indicate the number of slices. Additional horizontal plus vertical lines indicate the means ± SEM of the control burst rate for those slices tested for a specific agent. Note that the values correspond to the combined average burst rate of slices that showed a dual burst patterns (i.e., a eupnea–biphasic or a eupnea–sigh pattern).