Laryngeal constrictor motoneurons (LCMN) are activated during post-inspiration and act to slow expiratory airflow. However, little is known about how this phasic activity is generated. Here, we investigated the electrophysiological responses of identified LCMN to local application of GABA and bicuculline methiodide (BIC) in 14 anaesthetised Sprague-Dawley rats. During extracellular recordings, GABA iontophoresis (0.5 M) strongly inhibited LCMN (n = 6). Interestingly, BIC iontophoresis (5 mM) reduced, rather than increased, LCMN post-inspiratory activity (5 out of 6). Furthermore, intracellular recording revealed that BIC reduced not only the hyperpolarisation of the LCMN during inspiration (2.5 ± 1.4 mV before and 1.5 ± 0.4 mV after the BIC, P = 0.05, n = 5), but also the depolarisation during post-inspiration (3.0 ± 1.3 mV before and 1.6 ± 0.4 mV after the BIC, P = 0.02, n = 5). Our results demonstrate for the first time that the inspiratory inhibition of LCMN is primarily mediated by GABAA receptors. A possible involvement of a post-inhibitory rebound mechanism is discussed to explain how blockade of an inspiratory inhibition would affect LCMN excitability during post-inspiration.