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Department of Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73190
Submitted 8 October 2003; accepted in final form 19 December 2003
Because vagal and sympathetic inputs activate upper cervical spinal neurons, we hypothesized that stimulation of the esophagus would activate C1C2 neurons. This study examined responses of C1C2 spinal neurons to cervical and thoracic esophageal distension (CED, TED) and afferent pathways for CED and TED inputs to C1C2 spinal neurons. Extracellular potentials of single C1C2 spinal neurons were recorded in pentobarbital-anesthetized male rats. Graded CED or TED was produced by water inflation (0.10.5 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 C6C7 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 C6C7 spinal transection plus bilateral vagotomy eliminated responses of 2/2 neurons. Thus inputs from CED to C1C2 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 C1C2 spinal neurons play a role in integrating visceral information from cervical and thoracic esophagus.
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