The influence of immobilization stress upon the incidence of the episode of paradoxical sleep (PS) was studied both in mature ovariectomized and immature New Zealand White rabbits with electrodes implanted chronically in several parts of the brain.
The characteristic EEG changes of PS and animal's behavior as well as remarkable diminutions of electromyographic discharges from m. trapeziuspars cervicalis and m. scutuloauricularis superior were employed as indicators of the PS appearance, and the following sequences of PS have been observed. 1. The distribution of spontaneous PS episodes was markedly increased for 4-8 hours soon after the release of a 12 hours insomnia, reaching 2.1-5.5 times as large as that of pre-insomnia. In case of insomnia lasting nearly 24 hours, however, there was observed the merely 1.3-1.7 times increased distribution for 4-8 hours immediately after its release as compared with that of preinsomnia.
2. In the mature rabbit with immobilization stress imposed for 6 hours, the PS episode was depressed in a marked degree for 4-8 hours soon after its release; especially for the first 4 hours after release, almost no PS distribution was made. On the other hand, in case of the immature rabbit, there was hardly observed any blocking effect upon the distribution of PS.
3. Only a slight or almost no PS blocking phenomenon induced by the stress was observed in the rabbit implanted with minute amount of hydrocortisone in various regions of the brain such as the ant. median eminence, supraoptic region and the ventromedial hypothalamus.
4. The spontaneous PS was blocked nearly two hours after the intravenous administration of ACTH (0.5-1.0 u. s. p. u.), and the threshold of the electricallyinduced PS was also elevated about 10 times as high as that of pre-injection.
On the other hand, the PS was not blocked with hydrocortisone (0.8-2.0mg) or desoxycorticosterone (0.8-2.0mg) injected intravenously. Moreover, in case of adrenalectomized animals, there was observed the lesser distribution of the PS than the non-adrenalectomized without the administration of hydrocortisone and desoxycorticosterone. Further, from the facts that the distribution of PS episode was promoted by adrenalin (5-10γg), oxytocin (0.3-1.0 u.) and vasopressin (0.3-0.5 u.), the blocking effect of stress upon the PS appearance seems to be based not on increased ACH, but on the increase of ACTH in the blood.
5. Both in the intact and supracollicular transectioned rabbit, the blocking effect of insulin (1.0-2.0 u.) was exerted upon the spontaneous PS episode for 85-101 minutes after intravenous injection and the PS threshold from electrically stimulating the septum had significantly risen over 10 times as high as the initial level within one hour following administration of 1.0u. of insulin.
6. Repeated immobilization stress resulted in almost no PS blocking phenomenon after release from the 5th or 6th stress.

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A method to observe the average pattern of the amplified P wave is described. ECG was recorded on a magnetic analogue tape and then played back in reverse so that the falling phase of the R wave was capable of furnishing the required triggering voltage of the oscilloscope sweep. The reversed record was then amplified. The photographically superimposed curves represented the average P wave pattern. It was found that the PQ interval in human ECG was remarkably constant in normal condition and that notches of about the same size as noises were seen on the P wave. The significance of these notches was studied experimentally in the canine heart by placing the surface electrodes at various sites of the heart.

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The evoked potentials of the slow wave were recorded from the thalamus following the stimulation of the splanchnic nerve. The neuron discharges were also recorded from CM by using a micro-electrode. The experimental research thus performed on the perception of the viscero-sensory activityled to the following results.
1. The evoked potentials were found in VPL, MGmc and CM of the thalamus following the stimulation of the splanchnic nerve. The potentials showed the different characteristics according to the recording site.
2. The evoked potential in CM to the splanchnic stimulation had a long latency and showed a posttetanic occlusion following the tetanic stimulation of the splanchnic nerve. The evoked potential was not influenced by a transection of the dorsal spinal tract.
3. In recording the evoked potentials subsequent to the splanchnic and sciatic stimulations, somatotopic representation was observed in VPL, but it was not found in CM and MGmc. Convergence of the afferent transmission occurred in CM from both the splanchnic and sciatic nerves.
4. The spindle burst of 20-30 c. p. s. was recognized in the potential from CM following the tetanic stimulation of the splanchnic nerve. Recording site of the spindle burst was absolutely localized in CM. The spindle burst disappeared under light anesthesia.
5. The same type of the spindle burst was caused in the potential from CM also by strychnization to the cortex of the frontal lobe.
6. The spindle burst in the potential from CM caused by the splanchnic stimulation, was suppressed until disappearance by the entire decortication on both sides.
7. Stimulation of CM and the adjacent nuclei caused the recruiting response in the electrocorticogram.
8. The convergence of the afferent transmission in CM from the viscerosensory and the somato-sensory systems was confirmed by observing neuron discharge recorded with micro-electrode. The mechanisms of occurrence of the posttetanic occlusion and the spindle burst following the tetanic stimulation of the splanchnic nerve were clarified by recording from CM the spontaneous unitary action potential and the driven unitary action potential to a single volley of the splanchnic nerve.
According to these results, it is suggested that the reverberating circuit from the thalamus to the cortex with a focus in CM plays an important role in the viscero-sensory perception.

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1. When sartorius muscle was exposed to Ringer's solution to which both 1mM ryanodine and 80mM KCl were added, at 0.1mM ryanodine, a slow ryanodine, a slow ryanodine contracture occurred after a latent period of 20 to 30 minutes, and at 1mM ryanodine, a slow sustained one developed immediately after a phasic KCl-contracture.
2. Ryanodine had no effect on the myofibrillar ATPase activity and on the ATP-induced tension development of single glycerol-extracted muscle fiber.
3. Ryanodine did not inhibit the relaxing activity of effective eluate on myofibrils and that of microsomes on myofibrils or single fiber. The effect of preincubation of the microsomes with ATP was not affected by ryanodine.
4. The relaxed fiber by microsomes and the spontaneously relaxed fiber by further incubation after addition of calcium were not contracted by addition of ryanodine.
5. By ryanodine, the inhibitory effect of calcium on the relaxation of fiber by microsomes was slightly potentiated and the rate of spontaneous recovery was remarkably reduced. On the other hand, even in the presence of ryanodine, the complete relaxation was finally produced.
6. Ryanodine reduced markedly the rate of calcium binding by microsomes, but it had only slight effect on the maximal amount of calcium binding.
7. The duration, the rate and the amount of extra splitting of ATP by addition of calcium were affected by ryanodine, while the basic splitting of ATP was not done.

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1. The chorda tympani responses to stimulation of the tongue of rats by Land D-MSG, 5'-GMP, 5'-IMP. 5'-UMP and 5'-CMP were recorded.
2. The 5'-ribonucleotides were found to produce a response in the chorda tympani nerve at a very low concentration and the response was characterized by its marked sustained phase. The stimulating effectiveness was in the order of L-MSG>_D-MSG and 5'-GMP>5'-IMP>5'-UMP>5'-CMP.
3. A marked enhancement was observed in the response magnitude when a small amount of 5'-GMP or 5'-IMP was added to L-MSG or when a part of _L-MSG was substituted for an equal amount of 5'-GMP or 5'IMP.
4. Similar enhancement, though small, was observed in the response magnitude when 5'-UMP or 5'-CMP was added to _L-MSG.
5. No enhancement in the response magnitude was obtained either when 5-GMP and 5'-IMP were mixed together or when 5'-IMP or 5'-GMP was mixed with 5'-UMP or 5'-CMP.

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1. The relation between the change in surface negative cortical response of the rabbit during Nembutal anesthesia and the activity of individual neurons in the cortex was studied intracellulary or extracellulary with surface electrode and microelectrode. With Nembutal anesthesia the response increased in amplitude, and the form changed from monophasic to biphasic.
2. At the depth of 0.4mm from the surface spiky response composed of many units was evoked by surface stimulation. The number of unit spikes did not change or slightly decreased, even when the animal was anesthetized with Nembutal.
3. Among the spontaneously firing units there was a sort of neuron having intimate relation to EEG.
4. Spontaneously firing units were depressed for 50-300 msec by surface stimulation, the depressed period varied with the strength of stimulus at the surface. This depression was due to IPSP. With Nembutal anesthesia the duration of the period did not show any change.
5. The firing level of neurons in the cortex remained constant during Nembutal anesthesia, but deteriorated neurons showed the shift of firing level. The deteriorated neuron responded to direct transmembrane stimulating current passing through microelectrode with graded response, sometimes with oscillation of membrane potential.
6. The relation between the potential change at a point along dendrite neces sary to fire the cell and the distance from the initial segment was mathe matically derived. And the possibility, that the synapses near to the initial segment might be block with Nembutal anesthesia, was shown.

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Responses of single primary auditory neurons to electro-magnetic driving of the ear drum were studied. From the latency measurement of the responses of neurons for either attraction or repulsion of the ear drum, trigger action may result from basilar membrane displacement toward the scala vestibuli. The traveling wave occurs along the basilar membrane when a step function type of stimulus is applied to the ear drum electromagnetically. This means that the basilar membrane moves due to its natural vibration for the transient effect and does not respond to the steady phase of the stimulus.

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