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1. Single electrode voltage clamp recordings were obtained from myenteric neurones of guinea-pig ileum in vitro. Slow excitatory postsynaptic currents (sEPSCs) were elicited by focal stimulation of interganglionic nerve strands in twenty-four of thirty neurones more than 30 min after impalement. In seventeen of twenty-four neurones, sEPSCs were associated with a conductance decrease and reversed polarity at -96 ± 3 mV (near the reversal potential for potassium, E(K)); this response was due to inhibition of resting potassium conductance, g(K). In seven of twenty-four neurones, there was either no net conductance change or a biphasic conductance change during the sEPSC; a reversal potential for peak currents could not be determined. 2. Application of senktide (3 μM), a neurokinin-3 receptor agonist, caused an inward current in forty-one of fifty-three neurones more than 30 min after impalement. In twenty of forty-one neurones, senktide-induced currents were due to inhibition of resting g(K). In eleven of forty-one neurones there was either no net conductance change or a biphasic conductance change; a reversal potential for peak currents could not be determined. In ten out of forty-one neurones, senktide-induced currents were associated with a conductance increase (g(inc)); the estimated reversal potential was -17 ± 3 mV. 3. Application of forskolin (1 μM) caused an inward current that occluded the decrease in g(K) caused by senktide and the sEPSC. In neurones in which sESPCs and senktide responses were associated with an unclear or biphasic conductance change, forskolin did not reduce the peak current and residual currents were usually associated with a g(inc). 4. In neurones in which senktide-induced currents were associated with a g(inc), reducing extracellular Cl- to 13 mM reduced senktide-induced currents by 79%. Reducing extracellular Na+, or adding tetraethylammonium (TEA, 50 mM), cobalt (2 mM) or picrotoxin (30 μM) did not change senktide-induced currents. The chloride transport/ channel blockers niflumic acid and mefenamic acid (both at 100 μM) blocked senktide-induced currents. It was concluded that senktide increases chloride conductance (g(Cl)). 5. Chord conductance measurements made between -70 and -90 mV during sEPSCs were used to determine the contribution of an increase in g(Cl) to sEPSCs. These measurements indicated that the peak sEPSC is composed of a 90% decrease in g(K) and a 10% increase in g(Cl). Similar data were obtained from measurements made during senktide responses. It was concluded that senktide-induced currents and sEPSCs are due to a concurrent decrease in g(K) and an increase in g(Cl) in a subset of 3 myenteric neurones.