Hyoscine

The results support the idea that cell therapy might be used to treat motility disorders caused by missing or diseased enteric neurons. 100 ms was chosen because it consistently evoked responses in the muscle large enough to allow pharmacologic studies (Supplementary Figure 1).
We recorded 5À8 inhibitory or excitatory responses in the circular muscle cells evoked by each of electrical stimulation or light stimulation before addition of antagonists to the bath solution. A similar number of responses to each type of stimulation was recorded in the presence of antagonists before the reversibility of antagonists was tested after a wash period of at least 15 minutes. If the impalement were lost during recordings, a new impalement was made at the same location, taking advantage of the syncytial nature of the smooth muscle. Drugs used in the experiments were hyoscine, hexamethonium, nicardipine, pyridoxal phosphate-6-axophenyl-2 0 -4 0disulfonic acid (PPADS), nitro-L-arginine (NOLA), trinitrophenyladenosine 5 0 -triphosphate (TNP-ATP) (all from Sigma Aldrich, Castle Hill, NSW, Australia), and MRS 2179 (Abcam Biochemicals, Melbourne, Australia). Stock solutions of antagonists were initially made up in distilled water and diluted to working concentrations on the day of the experiment.

The following drugs were dissolved as stock solutions in water or ethanol before being diluted to the final concentrations in organ baths: tetrodotoxin (TTX, 0.6 M; Alamone Laboratories; Jerusalem, Israel), hexamethonium (100 M), hyoscine (1 M), N -nitro-L-arginine (L-NNA, 100 M), nicardipine (3 M), nifedipine (2 M), and 1-[(2-chlorophenyl)diphenylmethyl]-1H-pyrazole (TRAM-34, 3 M) all from Sigma-Aldrich, Castle Hill, Australia, and 5,6-dichloro-1ethyl-1,3-dihydro-2H-benzimidazol-2-one (DCEBIO, 3 M; Tocris; In Vitro Technologies, Noble Park, Australia).