AIM: Systemic administration of μ-opioids at clinical doses for analgesia decreases respiratory rate. MORs (μ-opioid receptors) within the PB (parabrachial) complex are potential targets. The purpose of this study was to define the pontine region in which MOR agonists produce bradypnea and to determine whether antagonism of MORs in this region reverses the bradypnea produced by systemic administration of clinically relevant concentrations of the MOR agonist remifentanil. METHODS: The effects of microinjections of agonist [D-Ala2, N-Me-Phe4, Gly-ol5]-enkephalin (DAMGO; 100 μM) and antagonist naloxone (NAL; 100 μM) into the dorsal rostral pons on the phrenic neurogram were studied in a decerebrate, vagotomized, ventilated, paralyzed canine preparation during hyperoxia. A 1-mm grid pattern of microinjections was used. The DAMGO-sensitive region extended from 5 to 7 mm lateral of midline and from 0 to 2 mm caudal of the inferior colliculus at a depth of 3–4 mm. Inspiratory and expiratory durations (TI and TE) and peak phrenic nerve activity (PPA) were measured from the phrenic neurogram. RESULTS: Microinjections of DAMGO in the region of the PBN (parabrachial nuclei) cause significant decreases in fB and microinjections of NAL in the same PB region completely reverse the bradypnea induced by systemically administered opioids at concentrations clinically relevant for analgesia. CONCLUSION: These results indicate that PB complex, which is a major relay center for converging visceral, nociceptive, and thermoreceptive information to the forebrain is a major site of opioid-induced respiratory depression. This study emphasizes the powerful role that the pontine PB-KF complex (parabrachial/Kölliker-Fuse) plays in the control of phase timing and breathing frequency.