1. Balloon distension of the duodenum 2 cm oral or anal to the sphincter of Oddi-duodenal junction elevated the amplitude of spontaneous sphincter of Oddi phasic contractions by 37-7 + 8-5 or 120-1 + 79-8%, respectively (mean + S.E.M., both n= 6, P< 0 05, Wilcoxon test). To further investigate this response, this study aimed to determine if: (i) electrical field stimulation (EFS) of the duodenum influences sphincter of Oddi activity; (ii) intramural nerves mediate the response; and (iii) nicotinic and/or muscarinic receptors are involved. 2. Electrical field stimulation (70 V, 0 5 ms; 5-60 Hz, 10-20 s) of the duodenal anterior serosal surface 2-4 cm oral or anal to the sphincter of Oddi-duodenal junction, produced excitatory responses in the sphincter of Oddi in anaesthetized Australian brush-tailed possums (n = 45). 3. These responses were frequency dependent, maximal at 30 Hz (n = 4) and abolished by tetrodotoxin (9 jug kg-' I.A.; n = 6), or by crushing the duodenum (n = 3). Hexamethonium bromide (30 mg kg-' i.v.) did not significantly alter the response to duodenal EFS either oral (n =6) or anal (n =8) to the sphincter of Oddi-duodenal junction. Atropine sulphate (30 jug kg-' i.v.) reduced the response to duodenal EFS oral and anal to the sphincter of Oddi-duodenal junction to 11P2 + 5-8 (n = 6) and 45 0 + 26-8% (n = 8), respectively (both P< 0 05).4. Bilateral cervical vagotomy and guanethidine infusion (10 mg kg-' over 15 min i.v.) did not significantly alter the responses to duodenal EFS (n = 7). 5. Excitatory intramural neural pathways between the sphincter of Oddi and the segment of duodenum 4 cm oral and anal to the sphincter of Oddi-duodenal junction have been demonstrated. These postganglionic pathways may involve muscarinic receptors.