Spontaneous contractions were recorded from the circular muscle layer at three sites along the isolated mouse colon. The interval between contractions was approximately 4.5 min. The mean duration of the contractions ranged from 26 sec in the distal colon to 45 sec in the proximal colon. Contractions migrating more than half the length of the colon were termed colonic migrating motor complexes (CMMCs). Over 90% of tissues demonstrated migration predominantly in an aboral direction. Hyoscine (10(-6) M) decreased the amplitude of the CMMCs by at least 40% but had no significant effect on the interval or duration of the CMMCs. Nifedipine (10(-6) M) significantly decreased the amplitude of the CMMCs by 95% but did not alter the duration or the interval between the CMMCs. Hexamethonium (5 x 10(-4) M) and tetrodotoxin (TTX; 2 x 10(-6) M) abolished all CMMC activity. TTX increased the resting tone of the preparations. Nitro-L-arginine (10(-4) M) increased the resting tone of the preparations and significantly decreased the interval between the CMMCs by approximately 80% but had no significant effect on the duration of the CMMCs. The results suggest CMMCs migrate predominantly in an aboral direction and are neurogenic in origin. Nitric oxide may be involved in maintaining inhibition of the muscle between CMMCs.

SUMMARY1. Intracellular microelectrodes have been used to record the electrical activity of smooth muscle cells of the circular layer from full length strips of mouse colon in vitro. The membrane potential was unstable and showed slow depolarizations (mean amplitude, 10-9 mV; mean frequency, 0-008 Hz; mean duration, 56-4 s).2. A variable number (mean fifty-six) of rapid oscillations in membrane potential (mean amplitude, 10-2 mV) with a frequency of approximately 2 Hz and a duration of approximately 400 ms were superimposed on each slow depolarization. Occasionally, action potentials arose from the rapid oscillations. The action potentials, but neither the slow depolarizations nor the rapid oscillations, were abolished by 1.0 utM-nifedipine.3. The majority of the slow depolarizations and the associated rapid oscillations migrated aborally along the colon at a velocity of between 0 5 and 1.5 mm s-1; in the distal colon the slow depolarization was often preceded by a small hyperpolarization.4. During the rising and plateau phase of the slow depolarization the amplitude of electrotonic potentials was decreased. Hyperpolarization induced by passing current during the slow depolarization increased the amplitude of the rapid oscillations.5. Transmural electrical stimulation (single pulses) in the presence of nifedipine evoked (1 mm anal to the stimulating electrodes) an inhibitory junction potential which was sometimes preceded by an excitatory junction potential. The amplitude. of the evoked inhibitory junction potential was decreased during the rising and plateau phase of the slow depolarization.6. The slow depolarization and the rapid oscillations were abolished by hexamethonium (500 /SM), morphine (1-10 /lM) and tetrodotoxin (3-1 /tM). Atropine 7. Atropine (3-5 /tM) and morphine (10 ,M) abolished the evoked excitatory junction potential whilst tetrodotoxin (3-1 /iM) abolished both the excitatory and the inhibitory junction potential.

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