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NEUROREGULATION AND MOTILITY

Different responsiveness of excitatory and inhibitory enteric motor neurons in the human esophagus to electrical field stimulation and to nicotine

¹Fundació de Gastroenterologia Dr. Francisco Vilardell, 08025 Barcelona; and ²Department of Surgery, Hospital de Mataró, 08304 Mataró, Spain

Submitted 23 December 2003 ; accepted in final form 3 March 2004

To compare electrical field stimulation (EFS) with nicotine in the stimulation of excitatory and inhibitory enteric motoneurons (EMN) in the human esophagus, circular lower esophageal sphincter (LES), and circular and longitudinal esophageal body (EB) strips from 20 humans were studied in organ baths. Responses to EFS or nicotine (100 µM) were compared in basal conditions, after N^G-nitro-L-arginine (L-NNA; 100 µM), and after L-NNA and apamin (1 µM). LES strips developed myogenic tone enhanced by TTX (5 µM) or L-NNA. EFS-LES relaxation was abolished by TTX, unaffected by hexamethonium (100 µM), and enhanced by atropine (3 µM). Nicotine-LES relaxation was higher than EFS relaxation, reduced by TTX or atropine, and blocked by hexamethonium. After L-NNA, EFS elicited a strong cholinergic contraction in circular LES and EB, and nicotine elicited a small relaxation in LES and no contractile effect in EB. After L-NNA and apamin, EFS elicited a strong cholinergic contraction in LES and EB, and nicotine elicited a weak contraction amounting to 6.64 ± 3.19 and 9.20 ± 5.51% of that induced by EFS. EFS elicited a contraction in longitudinal strips; after L-NNA and apamin, nicotine did not induce any response. Inhibitory EMN tonically inhibit myogenic LES tone and are efficiently stimulated both by EFS and nicotinic acetylcholine receptors (nAChRs) located in somatodendritic regions and nerve terminals, releasing nitric oxide and an apamin-sensitive neurotransmitter. In contrast, although esophageal excitatory EMN are efficiently stimulated by EFS, their stimulation through nAChRs is difficult and causes weak responses, suggesting the participation of nonnicotinic mechanisms in neurotransmission to excitatory EMN in human esophagus.

nicotinic receptors; inhibitory neurotransmitters; nitric oxide; apamin-sensitive neurotransmission; human esophageal motility

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