A5 noradrenergic neurons control sympathetic outflow, nociception, and respiration. The presence of ₂-adrenergic receptors (₂-ARs) in A5 cells has been suggested by immunohistochemistry. In the present experiments, we analyze the response of spinally projecting A5 cells to ₂-AR agonists, and we compare it with that of locus ceruleus (A6) neurons. Whole cell recordings were obtained from 52 spinally projecting neurons in the ventrolateral pons of neonate rats. Immunohistochemistry showed that 60% of the recorded cells were A5 cells. In A5 cells clamped at 55 mV, norepinephrine (NE) in the presence of the ₁-AR antagonist prazosin produced a Ba²⁺-sensitive outward current (20.4 ± 2.6 pA; n = 28). The ₂-AR-induced current reversed at the K⁺ equilibrium potential (E_K) at three different extracellular K⁺ concentrations. Replacement of 82% of the extracellular Na concentration with N-methyl-D-glucamine did not change the reversal potential. The 19 presumably noncatecholaminergic neurons responded weakly or not at all to NE (2.5 ± 0.6 pA outward current). Pontospinal A6 neurons (n = 11) were also recorded. Six A6 cells displayed large tetrodotoxin (TTX)-resistant membrane oscillations. In these cells, the current induced by ₂-AR stimulation did not reverse over the voltages tested (50 to 130 mV) or reversed at potentials more negative than E_K (less than 114 mV). In A6 neurons that did not display large oscillations (n = 5), the ₂-AR-induced current reversed at or close to the E_K (90 ± 1.6 mV). In conclusion, A5 cells, like locus ceruleus neurons, have ₂-ARs that may function as autoreceptors. In both cases, ₂-AR activation increases an inwardly rectifying K⁺ conductance. In A5 cells, we found no evidence that ₂-AR activation decreases a resting Na⁺ conductance. The inhibition of A5 cells by clonidine and other agents with ₂-AR agonist activity is likely to contribute to the ability of these drugs to decrease sympathetic tone and arterial pressure.