An in vitro brain stem preparation from adult turtles was used to determine effects of dopamine (DA) and norepinephrine (NE) on the pattern of respiratory motor output recorded from hypoglossal nerve roots (XII). Bath-applied DA (10-200 µM) increased the frequency of respiratory bursts (peaks) from 0.9 ± 0.2 to 2.4 ± 0.3 (SE) peaks/min, resulting in a 99 ± 9% increase in neural minute activity. R[+]-SCH-23390 (10 µM, D₁ antagonist) and eticlopride (20 µM, D₂ antagonist) attenuated the DA-mediated increase in peak frequency by 52 and 59%, respectively. On the other hand, the DA-receptor agonists apomorphine (D₁, D₂), quinelorane (D₂), and SKF-38393 (D₁) had no effect on peak frequency. Prazosin, an ₁-adrenergic antagonist (250 nM) abolished the DA-mediated frequency increase. Although NE (10-200 µM) and phenylephrine (10-200 µM, ₁-adrenergic agonist) increased peak frequency from 0.5 ± 0.1 to 1.2 ± 0.3 peaks/min and from 0.6 ± 0.1 to 1.0 ± 0.2 peaks/min, respectively, these effects were not as large as that with DA alone. The data suggest that both dopaminergic and adrenergic receptor activation in the brain stem increase respiratory frequency in turtles, but the DA receptor-mediated increase is dependent on coactivation of ₁-adrenergic receptors.