Abstract

The laryngeal adductor reflex (LAR) is a protective behavior induced by stimulation of upper airway afferents. Laryngeal afferent information reaches interneurons in the medulla via the superior laryngeal nerve (SLN). Expiratory laryngeal motoneurons (ELMs) are subsequently excited causing contraction of the thyroarytenoid (TA) and posterior cricoarytenoid (PCA) muscles. The LAR consists of a short latency (~10 ms), short duration (~10 ms) burst (R1) and a longer latency (~40ms) burst (R2) in laryngeal electromyogram (EMG) activity. We have shown that R1 LAR magnitude undergoes frequency‐dependent depression in response to electrical stimulation (eStim) of the SLN. Based on preliminary observations, we hypothesized that the R1 component of the LAR induced by SLN eStim oscillates. In anesthetized, spontaneously breathing cats (n=12: 7 males, 5 females), we recorded EMG activity from the TA bilaterally and the PCA unilaterally. The SLN was electrically stimulated at 2 or 20 Hz to evoke TA LAR ipsilateral to stimulation (iTA). No sex differences in TA or PCA LAR EMG magnitude were observed. Consistent with previous findings, TA LAR magnitude differed with breathing phase; normalized iTA LAR magnitude was 10% larger during expiration compared to inspiration. TA LAR contralateral to stimulation (cTA) and ipsilateral PCA LAR magnitudes were not breathing phase dependent. TA and PCA LAR EMG oscillations were highly variable across animals (range: 244 to 1140 Hz). Mean iTA EMG frequency was decreased at 20 Hz (2 to 20 Hz: 616 to 518 Hz, p=0.05). Mean cTA periodicity trended down at 20 Hz (2 to 20 Hz cTA: 647 to 531 Hz, p=0.07). In separate decerebrate, paralyzed cats (n=13), extracellular recordings of neurons in the ventral respiratory column (VRC) with multiple electrode arrays were conducted. Peristimulus time histograms provided evidence that ELMs oscillated at frequencies following SLN eStim similar to the lower range of periodicities in TA EMGs in unparalyzed animals. A subset of neurons recorded in the VRC were excited or inhibited by SLN eStim at short latencies. Spike train analysis suggested that ELM oscillations could be accounted for by synaptic inhibition and excitation from laryngeal‐responsive VRC inspiratory, expiratory, and non‐breathing modulated neurons. We conclude that the LAR is temporally regulated by a complex, anatomically distributed brainstem network that is capable of strong synchrony in response to stimulation of laryngeal afferents. We speculate that the function of this laryngeal‐responsive network is to exert tight regulatory control over LAR patterning.Support or Funding InformationSupported by NIH HL131716 and 3OT2OD023854

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