Abstract

Using a double sucrose gap method, inhibitory junction potentials (IJP) appeared in muscles of the circular layer of the large intestine in response to intramural stimulation in the presence of atropine. Under voltage clamp conditions, an inhibitory junction current (IJC) in the outward direction appeared in response to the same stimulus, declining exponentially 100–150 msec after the peak. The amplitude of IJC was a linear function of membrane potential; the reversal potential of the peak IJC was in the region of the potassium equilibrium potential. The time constant of decay (τ) depended exponentially on membrane potential, falling by a factor ofe on hyperpolarization by 120 mV. A decrease or increase in quantum composition of IJC caused a corresponding change in τ of IJC decay. Meanwhile apamine (5×10−7 g/ml) reduced the amplitude of IJC without affecting its kinetics. The action of ATP (10−3 M) led to a decrease in amplitude and τ of decay of IJC, evidently on account of occupation of some postsynaptic receptors by ATP. It is suggested that ATP facilitates the delayed diffusion of releasing mediator, by occupying synaptic receptors. Since an increase in the quantity of secreted mediator caused only a very small increase in the amplitude of IJC, it was postulated that under normal conditions the postsynaptic effect of the released mediator is close to maximal.

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