Abstract

Gastric and oesophageal afferent inputs to vagal efferent fibres were investigated in Urethane anaesthetized ferrets. Mechanical, chemical, and pharmacological stimuli were tested and efferent activity recorded from single cervical vagal fibres. Fibres showed either no basal discharge or low frequency, irregular patterns of resting discharge; only those which showed >50% excitation or inhibition of basal activity with both gastric distension and oesophageal balloon distension were studied further. These responses were rapid and maintained only for the duration of the stimuli. 18/32 efferent fibres tested also showed changes in discharge in response to acid infused slowly into the distal oesophagus. These responses were larger after repeated acid infusions. Subsequent intra-oesophageal capsaicin elicited a similar response in 7/8 fibres. These responses were reproducible with repeated capsaicin infusions in 2/4 fibres and desensitized in 2/4 fibres. 2 capsaicin-responsive fibres were unresponsive to oesophageal acidification. 4/12 fibres tested responded to close intraarterial injections of capsaicin and 9/12 to close intraarterial bradykinin. These responses were brief and of short latency. Vagal efferent responses to mechanical and chemical stimuli above were unchanged after the NK-1 receptor antagonist CP96,345 (4 mg/kg i.v.). Subsequently, bilateral vagotomy caudal to the recording site abolished the basal activity in 4/7 fibres. In the 3 fibres where spontaneous activity remained, none of these responded to oesophageal distension or intra-oesophageal acid (2/2 fibres tested) after vagotomy, whereas 2/2 fibres tested still responded to gastric distension. The response of 1 fibre to intraarterial bradykinin and capsaicin was unchanged by vagotomy. We conclude that vagal efferent neurones respond to gastro-oesophageal mechanical inputs and also receive convergent input from oesophageal acid-sensitive and gastrointestinal bradykinin- and capsaicin-sensitive afferents. These afferent inputs are not mediated via NK-1 receptors. There also exists a nonvagal afferent input onto vagal efferent neurones which is probably spinal and likewise non NK-1 receptor mediated.

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