Hypophonia is an early symptom in Parkinson's disease a that involves an increase in laryngeal muscle activity, interfering with voice production. Our aim was to use an animal model to better understand the role of different dopamine receptor subtypes in the control of laryngeal neurophysiology. First, we evaluated the combined effects of SCH23390-a D₁ receptor antagonist with a D₂ receptor antagonist (eticlopride) on laryngeal neurophysiology, and then tested the separate effects of selective receptor antagonists. Thyroarytenoid (TA) and gastrocnemius (GN) muscle activity was measured at rest and while stimulating the internal branch of superior laryngeal nerve (iSLN) to elicit the laryngeal adductor response (LAR) in alpha-chloralose anesthetized rats. Paired stimuli at different inter-stimulus intervals between 250 and 5000 ms measured central conditioning of the LAR. Changes in resting muscle activity, response latency, amplitude and LAR conditioning after each drug were compared with the saline control. SCH23390 alone increased the resting TA muscle activity (p < 0.05). With the combined SCH23390 + eticlopride or SCH23390 alone, response latency decreased (p < 0.01), amplitude increased (p < 0.01) and the test LAR was reduced at 2000 ms ISI (p < 0.01). No LAR changes occurred when eticlopride was administrated alone at a low dose and only a tendency to suppress responses was found at a high dose. No changes in GN muscle activity occurred in any of the groups. The results suggest that a loss of stimulation of D₁ receptors plays a significant role in laryngeal pathophysiology in PD.