Characterization of recurrent laryngeal nerve function in rats

37th Congress of IUPS (Birmingham, UK) (2013) Proc 37th IUPS, PCD115

Poster Communications: Characterization of recurrent laryngeal nerve function in rats

I. Naggar1, N. Mor1, K. Nakase1, P. Zolkind1, J. B. Silverman1, K. Sundaram1, M. Stewart1, R. Kollmar1

1. SUNY Downstate Medical Center, Brooklyn, New York, United States.

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The recurrent laryngeal nerve (RLN) is a branch of the vagus nerve that controls the movement of the vocal folds and arytenoid cartilages. Since it is damaged in 4-10% of thyroid surgeries, a better characterization of its function may aid in finding ways to repair the consequent vocal fold paralysis after damage. To this end, we developed methods to measure RLN function and vocal fold movement in rats under normal conditions, after nerve crush or cut, and upon RLN stimulation in rats. Rats were anesthetized with urethane 1.5 mg/kg intraperitoneally. Right RLN activity was recorded, along with electrical activity of the posterior crico-arytenoid and thyro-arytenoid muscles. A microsuspension laryngoscope was fashioned to visualize the arytenoid cartilages, and the deviation of the cartilages from the midline on video served as a quantitative measure of vocal fold function. Breathing was assessed by recording changes in resistance over a piece of conductive rubber wrapped around the thorax. Recordings from the above techniques were taken simultaneously during normal vocal fold function and after nerve crush or cut. Average waveforms of a single respiratory cycle during normal function and after nerve injury were calculated for each recording. The RLN was stimulated at 1, 2, 5, 10, 20, and 50 Hz with 1-millisecond pulses under normal and nerve injury conditions. A total of 31 adult rats were used in these experiments. Under normal conditions, we found rhythmic firing in the RLN that correlated in time with electromyogram (EMG) activity, vocal fold movement, and breathing. Cutting or crushing the right RLN resulted in normal breathing, but cessation of RLN and EMG activity, as well as paralysis of the ipsilateral arytenoid near the midline position. Stimulation of the distal RLN under normal and cut conditions caused arytenoid twitches that occurred upon each pulse in the 1-10 Hz range. At 20 or 50 Hz, the arytenoid moved to or stayed at the midline during stimulation. The development of quantitative techniques to study RLN function is an important step towards validating a rat model for RLN lesions. Normal RLN activity causes opening and closing of the arytenoids, but overstimulation of the RLN may overpower the adductor muscles and cause midline paralysis of the vocal folds. Our results have implications for the study of RLN regeneration after injury, as nerve impulses occurring after re-innervation may be similar to indiscriminate RLN stimulation.



Where applicable, experiments conform with Society ethical requirements.

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