Responses evoked by electrical stimulation of the brainstem reticular formation in the jaw-opening and hypoglossal motor nerves of an arterially perfused rat preparation.

The interneuronal system in the brainstem reticular formation plays an important role in elaborate muscle coordination during various orofacial motor behaviors. In this study, we examined the distribution in the brainstem reticular formation of the sites that induce monosynaptic motor activity in the mylohyoid (jaw-opening) and hypoglossal nerves using an arterially perfused rat preparation. Electrical stimulation applied to 286 and 247 of the 309 sites in the brainstem evoked neural activity in the mylohyoid and hypoglossal nerves, respectively. The mean latency of the first component in the mylohyoid nerve response was significantly shorter than that in the hypoglossal nerve response. Moreover, the latency histogram of the first component in the hypoglossal nerve responses was bimodal, which was separated by 4.0 ms. The sites that induced short-latency (<4.0 ms) motor activity in the mylohyoid nerve and the hypoglossal nerve were frequently distributed in the rostral portion and the caudal portion of the brainstem reticular formation, respectively. Such difference in distributions of short-latency sites for mylohyoid and hypoglossal nerve responses likely corresponds to the distribution of excitatory premotor neurons targeting mylohyoid and hypoglossal motoneurons.

Enhancement of swallowing motor activity by the ACE inhibitor imidapril in an arterially perfused rat preparation.

Pharmacological agents that elevate dopamine and substance P concentrations have been suggested to prevent aspiration pneumonia and improve impaired swallowing processes. However, little is known about the effects of such agents on swallowing activities induced in motor nerves innervating the pharyngeal and laryngeal muscles. In this study, we examined the effects of imidapril, cilostazol, and amantadine, which are often prescribed for swallowing disorders, on swallowing motor activity. We recorded the efferent activities of the cervical vagal nerve, hypoglossal nerve, and phrenic nerve using arterially perfused rats aged between 21-35 postnatal days. The vagal nerve activity was used for evaluation of swallowing motor activity. When 1.25 ml of distilled water was injected into the oral cavity, or the superior laryngeal nerve was electrically stimulated, synchronized swallowing bursts were evoked in the vagal and hypoglossal nerves, while inspiratory discharges were inhibited in all the recorded nerves. Administration of imidapril (60 ng/ml) but not cilostazol (2.5 µg/ml) and amantadine (200 ng/ml) to the perfusate increased the mean peak amplitude of orally evoked swallowing bursts in the vagal nerve. Such increase in the peak amplitude by imidapril was antagonized by the administration of the NK1 receptor antagonist aprepitant (5 µg/ml) or the D1 receptor antagonist LE300 (2.5 µg/ml). In contrast, neither imidapril nor cilostazol caused a significant increase in swallowing bursts evoked by electrical stimulation of the superior laryngeal nerve. These results suggest that imidapril treatment may improve impaired swallowing by enhancing pharyngeal muscle activities via an increase in substance P and dopamine concentrations.