Frequency Dependent Inhibitory Mechanisms Controlling the Laryngeal Adductor Response (LAR)

Abstract

Electrical stimulation of the superior laryngeal nerve (SLN) has been used to induce behaviors with airway protective components, such as the LAR. The LAR has both short (R1) and long latency (R2) peaks in response to stimulation, but the neuronal pathways that produce and modulate the LAR are not well understood. It has been reported that there exists a frequency‐dependent suppression of R2 for SLN stimulation frequencies above 2.5 Hz. The R1 can follow frequencies of electrical stimulation of the SLN approaching 200 Hz, suggesting a high fidelity of brainstem neuronal pathways, but to our knowledge there is no report on whether R1 exhibits frequency‐dependent depression. We hypothesized that the R1 would exhibit frequency‐dependent depression consistent with the existence of modulatory short latency inhibitory mechanisms. To test this hypothesis, we monitored EMG activity from the thyroarytenoid (TA) muscle and electrically stimulated the SLN unilaterally with a range of frequencies between 1 and 40 Hz. All frequencies employed induced both repetitive swallowing and LAR. The R1 peak of the LAR was time‐locked to each stimulus pulse (peak R1 latencies were 13.7±0.5 ms (5–10 Hz) and 14.2±0.6 ms (35–40 Hz)), and the R2 peak was not observed. Lower frequency stimulations (5–10 Hz) of the SLN elicited significantly higher LAR amplitudes (52.8 ±2.9 % max) than higher frequency stimulations (35–40 Hz; 36.8±3.2 % max). In other experiments, analysis of neuronal responses recorded in the ventral respiratory column revealed evidence of stimulus‐induced synchrony as well as disruption of concurrent functional relationships among respiratory‐modulated neurons. These observations suggest that more complex regulatory mechanisms exist in addition to frequency‐dependent depression of the LAR.Support or Funding InformationSupported by NIH HL 103415, HL 111215, HL109025.