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The preganglionic recurrent laryngeal motoneurons (PRLMs) dominate the neural control of almost allthe intrinsic laryngeal muscles.These neurons receive noradrenergic projection, and systemic administration of α2-adrenoceptor (α2-AR) agonists reportedly causes augmented expiratory activity of the recurrent laryngeal nerve, glottis closure and laryngogenic apnea, however the central mechanisms remain unknown.The present study aimed to test the hypothesis that activation of medullary α2-ARs causes disinhibition of the PRLMs, and via which causes glottis closure and laryngogenic apnea.