The esophagus is a relatively simple though vital organ. It consists of a two-layered muscular tube whose lumen is lined by squamous stratified epithelium. Beyond its roleofpropellingfoodfromthepharynxtothestomach by apropulsivecontraction wave representing the esophageal phase of deglutition (Conklin and Christensen
1994; Jean 2001), it is more and more recognized as a sensory organ from which a variety of respiratory and cardiovascular reflexes can be triggered, thus cooperating with the larynx in protecting the lower airways from aspiration (Barthélémy et al. 1996; Lang et al. 2002; Lang et al. 2001; Loomis et al. 1997; Medda et al. 2003).
In ruminants, there is additional antiperistalsis for regurgitation. During emesis, the esophagus is a merely passive conduit except for some antiperistalsis in its upper part. In the interval between swallows, both oral and aboral ends of the esophagus are tonically closed by the upper and lower esophageal sphincters, UES and LES respectively, while the tubular esophagus is flaccid and partly filled with air. Despite this apparent simplicity, neuronal control of esophageal functions is quite complex.
Esophageal swallowing requires the well-coordinated opening of the UES, oralto-aboral peristalsis, and opening of the LES. These events are organized by a central pattern generator in the brainstem and controlled by vago–vagal reflexes making the esophagus highly dependent on extrinsic vagal innervation (Bieger 1993; Chang et al. 2003; Conklin and Christensen 1994; Jean 2001; Miller 1986). In  addition, the esophagus contains, as all other organs of the gastrointestinal tract, enteric ganglia providing a local neuronal network for motility control (Conklin and Christensen 1994). Although the esophagus harbors some mucous glands, and its blood vessels receive both intrinsic and extrinsic innervation, the major task of the esophageal nerve tissue is motility control. Understanding the innervation of the esophagus is a prerequisite for successful treatment of a variety of disorders, e.g., dysphagia, achalasia, gastroesophageal reflux disease (GERD), and non- cardiacchestpain (Castelletal.2004; Clouseetal.1999; Orlando2003; Orlando 2004; Qualman et al. 1984; Storr and Allescher 1999). In particular, GERD with its high prevalence of more than 10% represents a significant health problem. This review aims at summarizing current knowledge of anatomy of esophageal innervation and will focus on peculiarities of motor innervation of striated esophageal muscle, i.e., enteric coinnervation, and possible involvement of vagal afferent neurons in myenteric ganglionic circuitry. For a more extensive coverage, in particular of the older literature and of functional and clinical data, the reader may
consult the classical handbook article by Stöhr (1957) or recent reviews (Chang et al. 2003; Conklin and Christensen 1994; Orlando 2003; Orlando 2004; Sengupta 2000) The vagus nerve and branches from the sympathetic trunk and the celiac ganglion provide motor, preganglionic parasympathetic, and postganglionic sympathetic input, and these elements also carry numerous afferent fibers projecting 2 Introduction to the brainstem and spinal cord (Aharinejad and Firbas 1989; Collman et al. 1992; Collman et al. 1993; Fryscak et al. 1984; Hudson and Cummings 1985; Khurana
and Petras 1991). A well developed ganglionated myenteric plexus is present in both smooth and striated muscle portions of the esophagus (Christensen and Robison 1982; Greving 1931; Gruber 1968). In the submucous plexus, ganglia are rare or even absent, especially in small mammals. Extrinsic motor innervation has to match the peculiar anatomy of the esophageal tunica muscularis which consists either entirely of striated muscle fibers or a mixture of striated and smooth muscle depending on the species. In contrast to the pharynx, the striated part of the esophagus also harbors a smooth muscle lamina muscularis mucosae which typically separates the mucosa from the submucosa all along the gastrointestinal tract