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SUMMARY1. The inhibitory innervation of the taenia of the guinea-pig caecum has been studied, after blocking the responses to stimulation of excitatory cholinergic nerves with atropine.2. Stimulation of the perivascular nerves supplying the taenia caused relaxations. These nerves had properties which were typical of sympathetic post-ganglionic adrenergic nerves. The relaxations caused by stimulation were maximal at frequencies of stimulation above 30 pulses/sec and they were abolished by bretylium, guanethidine and l,l-dimethyl-4-phenylpiperazinium iodide (DMPP).3. The taenia is also innervated by intramural inhibitory nerves with their cell bodies in Auerbach's plexus. These nerves can be excited by electrical stimulation ofthe taenia or by the application ofganglion-stimulating drugs.4. The intramural inhibitory nerves have different properties from sympathetic adrenergic nerves. Relaxations in response to stimulation were maximal with frequencies of stimulation of about 5 pulses/sec and they were not blocked by bretylium, guanethidine or DMPP.5. Preganglionic cholinergic fibres in the caecal wall make synaptic connexions with the intramural inhibitory neurones.6. The role of the intramural inhibitory neurones in intestinal activity and their possible connexions with the central nervous system have been discussed.

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SUMMARY1. The effects of vagal stimulation and applied acetylcholine were compared on the isolated sinus venosus preparation of the toad, Bufo marinus.2. The effects of applied acetylcholine and of low-frequency, or short bursts of high-frequency vagal stimulation were abolished by hyoscine.3. When intracellular recordings were made from muscle cells of the sinus venosus, it was found that applied acetylcholine caused bradyeardia and a cessation of the heart beat which was associated with membrane hyperpolarization and a reduction in the duration of the action potentials. Much of the effect of acetylcholine can be attributed to it causing an increase in potassium conductance, 9K.4. When slowing was produced by low-frequency vagal stimulation, only a small increase in maximum diastolic potential was detected. During vagal arrest the membrane potential settled to a potential positive of the control maximum diastolic potential.5. In the presence of barium, much of the bradyeardia associated with vagal stimulation persisted. Although the bradycardia produced by added acetylcholine also persisted in the presence of barium, the effects of acetylcholine that could be attributed to an increase in gK were abolished.6. Addition of caesium ions produced bradyeardia with membrane potential changes similar to those seen during vagal stimulation.7. The results are discussed in relation to the idea that neuronally released acetylcholine reduces inward current flow during diastole. In contrast applied acetylcholine as well as reducing inward current flow during diastole also increases outward current flow by increasing 9