Figure 5.

Acute inhibition of AlstR-expressing Phox2b neurons in the ventrolateral brainstem prevents CO₂-induced postinspiratory vagal and late-expiratory abdominal discharges in situ. A, Changes in resting HN, cVN, AbN, and PN activities following allatostatin (1 μm) administration via the perfusate in an in situ preparation from an animal transduced with PRSx8-AlstR-EGFP-LV in the ventrolateral brainstem. Note reversible reduction of inspiratory and postinspiratory (arrow) activities; the latter accounts for the increase in respiratory frequency. B, The response to 8% CO₂ in the absence and presence of allatostatin; note the almost complete abolition of AbN late expiratory activity (arrows) and partial suppression of postinspiratory cVN activity. The reduction in inspiratory amplitude was less than that seen in normocapnia (see A). C, Summary data showing the effect of allatostatin on CO₂-induced increases in phrenic nerve amplitude, postinspiratory cVN activity, and numbers of AbN late-expiratory (late-E) bursts in preparations from the animals transduced with PRSx8-AlstR-EGFP-LV (AlstR) or PRSx8-EGFP-LV (EGFP) in the ventrolateral brainstem. *p < 0.05. Allatostatin application in non-LVV injected rats or rats transduced with PRSx8-EGFP-LV did not produce changes in respiratory motor outputs (data not shown).