Because vagal and sympathetic inputs activate upper cervical spinal neurons, we hypothesized that stimulation of the esophagus would activate C1-C2 neurons. This study examined 1) responses of C1-C2 spinal neurons to cervical and thoracic esophageal distension (CED, TED), and 2) afferent pathways for CED and TED inputs to C1-C2 spinal neurons. Extracellular potentials of single C1-C2 spinal neurons were recorded in pentobarbital anesthetized male rats. Graded CED or TED was produced by water inflation (0.1-0.5 ml) of a latex balloon. CED changed activity of 48/219 (22%) neurons; 34 were excited (E), 12 were inhibited (I), and 2 were E-I. CED elicited responses for 18/18 neurons tested after ipsilateral cervical vagotomy, for 12/14 neurons tested after bilateral vagotomy, and for 9/11 neurons tested after bilateral vagotomy and C6-C7 spinal cord transection. TED changed activity of 31/190 (16%) neurons (28E, 3 I). Ipsilateral cervical vagotomy abolished TED-evoked responses of 5/12 neurons. Bilateral vagotomy eliminated responses of 2/4 neurons tested and C6-C7 spinal transection plus bilateral vagotomy eliminated responses of 2/2 neurons. Thus, inputs from CED to C1-C2 neurons most likely entered upper cervical dorsal roots, whereas inputs from TED were dependent on vagal pathways and/or sympathetic afferent pathways that entered the thoracic dorsal roots. These results supported a concept that C1-C2 spinal neurons play a role in integrating visceral information from cervical and thoracic esophagus.