Читать книгу The Esophagus - Группа авторов - Страница 128

Motor innervation to the striated muscle esophagus originates in motor neurons of the nucleus ambiguus and is carried to the esophagus largely by the recurrent laryngeal nerve. The nerve fibers terminate in motor endplates in both circular and longitudinal layers [140] and release acetylcholine to contract the muscle through nicotinic muscarinic receptors [141]. The ganglion cells in the myenteric plexus send fibers to the motor endplates and contain NO, vasoactive intestinal peptide (VIP), galanin, and neuropeptide Y [142–146]. This coinnervation provides inhibitory modulation of striated muscle contraction and peristalsis through local and/or central reflexes [145, 146]. It is unclear whether vagal fibers from the SPG impact these neurons. IGLEs, considered to be sensory receptors, are present. ICCs are also present, but their role is unclear, although they may also function as sensory receptors 131, 147]. The region also receives sympathetic innervation, and sympathetic sensory information is passed from this region through segments C1–T8. 127].

Contraction of the striated muscle for both primary and secondary peristalsis is under central control of the SPG esophageal stage [5, 7, 35], with sequential excitation through vagal fibers [39, 40, 148]. This activity is sensitive to sensory feedback and may be modulated by local and/or central reflexes [145, 146, 149].