Abstract

The neurophysiological basis of esophageal pain and discomfort is not well known. Functional disorder, such as noncardiac chest pain, is thought to be associated with hypersensitivity of primary afferents innervating the esophagus and/or sensitization of spinal dorsal horn cells receiving input from the organ. Although we have accumulated a large body of information about the morphologic structure and neuropeptide contents of the extrinsic primary afferents, we lack a full understanding of its integrative function in esophageal pain. The esophagus is innervated dually by vagus and spinal nerves. The majority of sensory afferents in the vagal and spinal pathway are pseudounipolar cells, with their cell bodies (soma) located in the nodose and dorsal root ganglia, respectively. These afferent fibers innervate serosa (adventitia), longitudinal and circular muscles, and mucosa of the esophagus. Afferents innervating the muscle are sensitive to intraluminal distension. In the vagus, these afferents exhibit low threshold for response, whereas the spinal afferents, including the splanchnic nerve afferents, have either low or high thresholds for response. In addition, these afferents are chemosensitive. Both vagal and spinal afferents also innervate the mucosa of the esophagus. These fibers are exquisitely sensitive to light touch of the mucosa and are sensitive to pH and chemicals. The spinal afferents, including splanchnic nerve afferents, project to the spinal cord, spanning from upper cervical (C1) to upper lumbar (L2) segments. A majority of the spinal dorsal horn neurons receiving input from the esophageal spinal afferents also receives somatic converging input. The somatic receptive fields are distributed mainly ipsilaterally over the chest and forearm area. These spinal dorsal horn neurons exhibit either excitatory, inhibitory, or biphasic (i.e., excitation followed by inhibition) responses to esophageal distension.

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