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DOI 10.1016/j.job.2026.100816

Медицинская библиотека · Journal of oral biosciences · 2026

Role of the gigantocellular reticular nucleus in suppression of the swallowing reflex during stimulation of the pedunculopontine tegmental nucleus.

Oshikiri Yui, Satoh Yoshihide, Oohashi Makoto

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Аннотация

OBJECTIVES

A previous study reported that stimulation of the pedunculopontine tegmental nucleus (PTg) and the gigantocellular reticular nucleus (Gi) suppressed and modulated the swallowing reflex, respectively. The swallowing central pattern generator comprises the nucleus of the solitary tract (Sol) and lateral reticular formation (LRF). The PTg projects to the Gi, and the Gi projects to the Sol and LRF. Thus, suggesting that PTg-induced suppression of the swallowing reflex is mediated via the Gi. We investigated whether electric lesions of the Gi, or microinjection of methyllycaconitine (MLA), -an α7 nicotinic acetylcholine receptor antagonist, -into the Gi, affect PTg-induced suppression of the swallowing reflex.

METHODS

Experiments were performed on urethane-anesthetized rats. The swallowing reflex was evoked by repetitive electrical stimulation of the superior laryngeal nerve, and responses were recorded from the mylohyoid muscle using electromyography. The PTg was stimulated electrically. Following confirmation of PTg-induced suppression of the swallowing reflex, electric lesions of the Gi or injection of MLA into the Gi were performed.

RESULTS

Electric lesions of the Gi or injection of MLA into the Gi each reduced PTg-induced prolongation of the onset latency of the first swallow.

CONCLUSIONS

These results suggest that prolongation of the onset latency of the first swallow, induced by stimulation of the PTg, is mediated by a relay through the Gi.

Для цитирования: Oshikiri Yui, Satoh Yoshihide, Oohashi Makoto. Role of the gigantocellular reticular nucleus in suppression of the swallowing reflex during stimulation of the pedunculopontine tegmental nucleus.. Journal of oral biosciences. 2026. DOI: 10.1016/j.job.2026.100816.

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