Opiates have effects on respiratory neurons that depress tidal volume and air exchange, reduce chest wall compliance and slow rhythm. The most dose-sensitive opioid effect is slowing of the respiratory rhythm through mechanisms that have not been thoroughly investigated. An in vivo dose-response analysis was performed on medullary respiratory neurons of adult cats to investigate two untested hypotheses related to mechanisms of opioid-mediated rhythm slowing: (1) Opiates suppress intrinsic conductances that limit discharge duration in medullary Inspiratory and Expiratory neurons, (2) Opiates delay the onset and lengthen the duration of discharges postsynaptically in phase-regulating Post-Inspiratory (Post-I) and Late-Inspiratory (Late-I) neurons. In anesthetized and unanesthetized decerebrate cats, a threshold dose (3 µg/kg) of the µ-opioid receptor agonist fentanyl slowed respiratory rhythm by prolonging discharges of Inspiratory and Expiratory bulbospinal neurons. An additional 2-4 µg/kg also lengthened the inter-burst silent periods in each type of neuron and delayed the rate of membrane depolarization to firing threshold. These changes took place without altering synaptic drive potential amplitude, input resistance, peak action potential frequency, action potential shape or afterhyperpolarization. Fentanyl also prolonged discharges of Post-I and Late-I neurons in doses that slowed the rhythm of inspiratory and expiratory neurons, without altering peak membrane depolarization and hyperpolarization, input resistance or action potential properties. The temporal changes evoked in the tested neurons can explain the slowing of network respiratory rhythm, but the lack of significant, direct opioid-mediated membrane effects predicts actions emanating from other types of upstream bulbar respiratory neurons to account for rhythm slowing.