Background/aims: Little is known about the mechanisms controlling colonic migrating electrical activity. This study investigates the neural processes involved in the generation of migrating myoelectric complexes in the isolated mouse colon.
Methods: Intracellular electrophysiological recordings were obtained from the circular muscle layer of the mouse colon in vitro in the presence of 2 mumol/L nifedipine.
Results: Complexes occurred approximately every 3 minutes and consisted of 1 mumol/L hyoscine-sensitive rapid oscillations (approximately 2 Hz) superimposed on a slow depolarization (approximately 17 mV); the latter was often preceded by a precomplex hyperpolarization (approximately 7 mV) that was reduced by 250 nmol/L apamin. Five hundred micromolars of hexamethonium or 2 mumol/L of tetrodotoxin abolished the complexes and depolarized the muscle by 8.7 +/- 1.3 mV (n = 9) or 12.1 +/- 1.4 mV (n = 5), respectively. Carbachol (50 nmol/L to 5 mumol/L) produced dose-dependent depolarizations but without rapid oscillations. The nitric oxide synthase inhibitor NG-nitro-L-arginine (100 mumol/L) depolarized the tissue by 17.2 +/- 1.6 mV (n = 8) but had no effect on the rapid oscillations. In the presence of 2 mumol/L tetrodotoxin, 5 mumol/L sodium nitroprusside produced a sustained hyperpolarization (15.5 +/- 2.0 mV; n = 5) but did not restore complexes.
Conclusions: In the isolated mouse 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 simultaneous activation of cholinergic motor nerves.