Key points Laryngeal adduction is a major mechanism in sealing off entry to the trachea to prevent aspiration during swallowing. An experimental protocol to reliably elicit sequential swallowing by oral injection of small volumes of water was developed in the in situ perfused brainstem preparation of juvenile rats. The sequential swallowing motor pattern consists of two distinct components: (i) phasic swallowing, indicated by rhythmic sequential vagal nerve bursting, and (ii) protective laryngeal adduction, indicated by background tonic vagal discharge. Pharmacological manipulation of the Kölliker–Fuse nucleus revealed that it specifically mediates the protective tonic laryngeal adduction, while GABAergic neurotransmission is needed in the nucleus of the solitary tract for the generation of the sequential swallowing motor pattern. We conclude that sequential swallow motor patterning, including effective airway protection, requires balanced excitatory–inhibitory synaptic interaction within the nucleus of the solitary tract and the Kölliker–Fuse nucleus, as well as between the two nuclei. Abstract Both swallowing and respiration involve postinspiratory laryngeal adduction. Swallowing‐related postinspiratory neurons are likely to be located in the nucleus of the solitary tract (NTS) and those involved in respiration are found in the Kölliker–Fuse nucleus (KF). The function of KF and NTS in the generation of swallowing and its coordination with respiration was investigated in perfused brainstem preparations of juvenile rats (n = 41). Orally injected water evoked sequential pharyngeal swallowing (s‐PSW) seen as phasic, spindle‐shaped bursting of vagal nerve activity (VNA) against tonic postinspiratory discharge. KF inhibition by microinjecting isoguvacine (GABAA receptor agonist) selectively attenuated tonic postinspiratory VNA (n = 10, P < 0.001) but had no effect on frequency or timing of s‐PSW. KF disinhibition after bicuculline (GABAA receptor antagonist) microinjections caused an increase of the tonic VNA (n = 8, P < 0.01) resulting in obscured and delayed phasic s‐PSW. Occurrence of spontaneous PSW significantly increased after KF inhibition (P < 0.0001) but not after KF disinhibition (P = 0.14). NTS isoguvacine microinjections attenuated the occurrence of all PSW (n = 5, P < 0.01). NTS bicuculline microinjections (n = 6) resulted in spontaneous activation of a disordered PSW pattern and long‐lasting suppression of respiratory activity. Pharmacological manipulation of either KF or NTS also triggered profound changes in respiratory postinspiratory VNA. Our results indicate that the s‐PSW comprises two functionally distinct components. While the primary s‐PSW is generated within the NTS, a KF‐mediated laryngeal adductor reflex safeguards the lower airways from aspiration. Synaptic interaction between KF and NTS is required for s‐PSW coordination with respiration as well as for proper gating and timing of s‐PSW.