NEUROGENIC CONTROL OF MYOELECTRIC COMPLEXES IN THE MOUSE ISOLATED COLON

Background/Aims: Little is known about the mechanisms controlling colo nic migrating electrical activity. This study investigates the neural processes involved in the generation of migrating myoelectric complexe s in the isolated mouse colon. Methods: Intracellular electrophysioiog ical recordings were obtained from the circular muscle layer of the mo use colon in vitro in the presence of 2 mu mol/L nifedipine. Results: Complexes occurred approximately every 3 minutes and consisted of 1 mu mol/L hyoscine-sensitive vapid oscillations (similar to 2 Hz) superim posed on a slow depolarization (similar to 17 mV); the latter was ofte n preceded by a precomplex hyperpolarization (similar to 7 mV) that wa s reduced by 250 nmol/L apamin. Five hundred micromolars of hexamethon ium or 2 mu mol/L of tetrodotoxin abolished the complexes and depolari zed the muscle by 8.7 +/- 1.3 mV (n = 9) or 12.1 +/- 1.4 mV (n = 5), r espectively. Carbachol (50 nmol/L to 5 mu mol/L) produced dose-depende nt depolarizations but without vapid oscillations. The nitric oxide sy nthase inhibitor N-G-nitro-L-arginine (100 mu mol/L) depolarized the t issue by 17.2 +/- 1.6 mV (n = 8) but had no effect on the rapid oscill ations. In the presence of 2 mu mol/L tetrodotoxin, 5 mu mol/L sodium nitroprus-side produced a sustained hyperpolarization (15.5 +/- 2.0 mV ; n = 5) but did not restore complexes. Conclusions: In the isolated m ouse colon, the membrane potential between complexes is maintained by the release of inhibitory neurotransmitters (including nitric oxide), and the formation of complexes involves disinhibition and the simultan eous activation of cholinergic motor nerves.