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 micrograms kg-1 I.A.; n = 6), or by crushing the duodenum (n = 3). Hexamethonium bromide (30 mg kg-1 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 micrograms kg-1 I.V.) reduced the response to duodenal EFS oral and anal to the sphincter of Oddi-duodenal junction to 11.2 +/- 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-1 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.