Varicosities of nitrergic and other nerves end on deep muscular plexus ICC or on CD34 positive, c-kit negative fibroblast-like cells. Both cell types connect to outer circular muscle by gap junctions, which may transmit nerve messages to muscle. We tested the hypotheses that gap junctions transmit pacing messages from ICC of the myenteric plexus. Effects of inhibitors of gap junction conductance were studied on paced contractions and nerve transmissions in small segments of circular muscle of mouse intestine. Using electrical field stimulation parameters (50V/cm, 5pps, and 0.5 ms) which evoke near maximal responses to nitrergic, cholinergic and apamin-sensitive nerve stimulation, we isolated inhibitory responses to nitrergic nerves, inhibitory responses to apamin-sensitive nerves and excitatory responses to cholinergic nerves. 18 glycyrrhetinic acid (10, 30 and 100 µM), octanol (0.1, 0.3, and 1 mM) and gap peptides (300 µM of ⁴⁰Gap 27, ⁴³Gap26, ^37,43Gap27) all failed to abolish neuro-transmission. 18 glycyrrhetinic acid inhibited frequencies of paced contractions, likely due to inhibition of L-type Ca²⁺ channels in smooth muscle, but octanol or gap peptides did not . 18 glycyrrhetinic acid and octanol, but not gap peptides, reduced the amplitudes of spontaneous and nerve-induced contractions. These reductions paralleled reductions in contractions to exogenous carbachol. Additional experiments with gap peptides in both longitudinal and circular muscle segments after L-NNA and TTX revealed no effects on pacing frequencies. We conclude that gap junction coupling may not be necessary for pacing or nerve transmission to the circular muscle of the mouse intestine.