The cervial vagus nerves of the mammalians are known to be composed of the fol lowing five, functionally different fibers: 1) general somatic afferent fibers, 2) general visceral afferent fibers, 3) specific visceral afferent fibers, 4) general visceral efferent fibers and 5) specific visceral efferent fibers (1). The general visceral efferent fibers originating from the dorsal motor nucleus of the vagus in the medulla oblongata are regarded to be cholinergic in nature. But fluorescence histochemical studies showed that green-fluores cent noradrenaline terminals became visible in the part of this nucleus after giving 1-dopa to rats (2).Cholinergic impulses conducted in the vagus nerve give rise to the inhibition of cardiac rate and contractility, the relaxation of gastrointestinal sphincters and also to the increase of gastrointestinal motility and tone. However, since the demonstration by McEwen (3) that electrical stimulation of the vagus nerve to the isolated rabbit atria resulted in the increase in cardiac rate and contractility under the presence of hexamethonium, evi dence to confirm the dual responses of the heart to vagal stimulation is accumulating in cats (4), rabbits (5-7) and guinea pigs (8) under various experimental conditions. Jellinek et al. (9) have shown that bilateral cervical vagosympathectomy results in a significant reduction of cardiac catecholamine if dogs survived surgery. The results are rather indicative of the contribution of the vagus nerves to retaining the endogenous noradrenaline in the heart. The demonstration by Hamberger and Norberg (10) that the pelvic nerve of the cat, known to be pure cholinergic in nature, contained the nora drenaline-fluorescent fibers stimulated the authors to perform the present experiments.The vagus nerve of the cat, readily separable from the cervical sympathetic nerve, and also the same nerve of the dog constituting the vagosympathicus were found to contain the noradrenali ne-fluorescent fibers. METHODS

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It has been well-known that the electrical activity of the central nervous system is facilitated by relatively lower doses of central depressants.Many reports were presented to support the facilitatory mechanism in the brain of exprimental animals at lower dose levels of barbiturates : lowering of stimulation threshold for the recruiting response by King (1) and' Domino (2), increase in amplitude of the somatosensory evoked poten tial recorded from the internal capsule by King et al. (3), and increase in amplitude of the evoked potential recorded from the auditory cortex by Pradhan and Galambos (4).Nakai (5) and Nakai and Takaori (6) showed that pentobarbital sodium, chloralose and chlorpromazine increased the magnitude of the cortical potential evoked by click stimuli and accelerated the manifestation of the ensuing rhythmic after-discharges, while urethane and ethyl alcohol even in small doses reduced the amplitude of the evoked potential.The role of the inferior colliculus as a relay nucleus for the auditory pathway was investigated electrophysiologically by Ades and Brookhart (7) and Thurlow et al. (8).However, there is scarcely any systematic study concerning the effects of central depres sants on the evoked potential in the inferior colliculus. It is considered that the effect of central depressants on the collicular acoustic potential may differ from that on the cortical one. The difference may give some clue for the elucidation of the central audi tory mechanism. METHODSAll experiments were performed in a sound-proof room maintained at the tempera ture of 27°C using cats weighing 2.0 to 3.5 kg. Under ether anesthesia the exposed trachea was intubated and the head of animal was fixed on the stereotaxic instru ment of Todai-Noken type.The left occipital skull covering the cerebrum and cerebellum was , removed, and the left tentorium cerebelli was carefully resected. The left inferior colliculus was exposed for insertion of the recording electrode under direct inspection. The cerebral and cerebellar corticies were not removed. Thereafter, the spinal cord was sectioned at the level of C1 (encephale isole preparation) and the animal was maintained by artificial respiration. A monopolar insulated silver electrode, about

It is generally believed that the cardiac fibers of the right vagus nerve terminate , in large part, near the sinoatrial node and some fibers distribute widely in the atria , and that most of the cardiac fibers of the left vagus supply the atrioventricular node and bundles.On the other hand, there are opposite conclusions regarding the existence of the vagus nerve endings in the ventricles. Electrical stimulation of the vagal fibers to the heart has usually been performed in the open chest animal or in the heart-lung preparation of the dog. Many investigators agree with the inhibitory nature of the vagal innervation on the heart, while there is some evidence for existence of the cardio-accele rator fibers in the vagus nerve (1-4). Middleton et al . (5) have concluded that some vagal fibers make connection with the chromaffin cells or the adrenergic neurons located in or near the heart by demonstrating an adrenaline-like substance in the perfusate of the cat's heart which is responding with the increase in rate and amplitude to vagal stimulation. McEwen (6) has observed an inhibitory effect of vagal stimulation in the rabbit's heart for many hours after the isolation.He , further, has demonstrated that the vagal stimulation restores the normal rhythmicity of contraction in the atria arrested by suspending in the bath for many hours , and that the same vagal stimula tion inihibits the regular rhythm restored by the addition of acetylcholine . Using the same type of preparations, Burn and Rand (7) have observed the restarting effect of vagal stimulation on the heart which ceased to beat by cooling.The marked acceleration of the repolarization phase in the atrial membrane poten tials of the dog's and rat's hearts in situ following vagal stimulation has been shown by Hoffman and Suckling (8) and Biersteker et al. (9). Similar observation was made on the turtle's heart in situ by Churney et al. (10). Although the vagal effect on the membrane potentials of the isolated frog's heart was demonstrated by Hutter and Trautwein (11), the vagal effect on the atrial or ventricular membrane potentials of the isolated mammalian heart has not hitherto been presented. During the study of the effect of va,al stimulation on the transmembrane potentials (12) , the authors have been confronted with many difficulties which should be previously removed in the iso-