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The recurrent laryngeal nerve (RLN) commonly regenerates after injury; however, functional motion is rarely recovered. Animal experiments have documented aberrant reinnervation after nerve transection, with motor axons reaching inappropriate muscles. More recently, experimental results suggest that lack of vocal fold motion after RLN injury is due to preferential reinnervation of adductor muscles, with inadequate reinnervation of the posterior cricoarytenoid muscle (PCA), the only abductor muscle of the larynx. Information on factors that could influence the receptiveness of these muscles to reinnervation could be useful in developing new therapeutic strategies. It is hypothesized that the thyroarytenoid muscle (TA) and the PCA differ in expression of neurotrophins in response to denervation.Laboratory experiment.Rats were sacrificed at 3 days, 6 weeks, or 4 months after unilateral RLN injury measure expression of brain-derived nerve growth factor (BDNF), nerve growth factor (NGF), and neurotrophin 4 (NT-4) in the TA and PCA muscles, using immunohistochemistry. We also assessed nerve regeneration.NGF was significantly diminished in the denervated TA muscle at 3 days after injury and increased at 6 weeks. BDNF expression was unchanged in the TA, but was diminished in both PCA muscles at 3 days and 6 weeks, returning to near-normal levels at 4 months after injury. Robust nerve regeneration of distal RLN was present at 4 months.Results suggest that the TA and PCA muscles respond differently to denervation.