1. The effects of electrical stimulation of the pericruciate cortex on individual neurons of the ventrobasal complex (VB) of the thalamus has been studied in cats. Extracellular recording was via glass micropipettes. Unit spikes were evoked by single test shocks applied either to peripheral nerves or to the medial lemniscus.
2. About half the neurons tested were excited antidromically by single shocks to restricted areas of the postcruciate cortex. Similar stimulation caused trans-synaptic excitation in about one third of the neurons.
3. When these and adjacent areas of postcruciate cortex were weakly stimulated prior to the medial lemniscal test shock, the VB unit was commonly inhibited. The inhibitory effect usually lasted 300 msec. or more.
4. Some VB neurons were excited by stimulation of the ipsilateral pyramid at the ponto-bulbar border. The specificity of this pyramidal stimulation was checked by monitoring antidromically evoked cortical potentials.
5. Twenty-two to 30 days following cortical ablation, with degenera tion of the descending pyramidal fibers, stimulation of the exposed subcortical white matter had an antidromic inhibitory effect on the VB neurons. No transsynaptic excitation was produced in these cases either by stimulation of subcortical white matter or the medullary pyramid.
6. These results suggest that some axon collaterals of pyramidal tract fibers project to the VB complex and produce excitation of small groups of VB neurons, which in turn results in inhibition of surrounding VB neurons. Possible functional significance of the results was briefly discussed.

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1. Employing the original as well as modified Trendelenburg's method and the intraluminal perfusion method the motility of the isolated small intestine of guinea pigs is studied.
2. The evidences have been obtained that the preparatory phase is entirely of a physical nature, and that the preceding longitudinal shortening is produced because the loop is stretched along its longitudinal axis.
3. With the increase of the intraluminal pressure the contraction waves are gradually increased in their strength and regulated to propagate from oral to anal, that is, coordinated, without showing any definite changes both in their period and velocity of propagation. On the basis of the results described above the concept according to which the critical intraluminal pressure produces an entirely new pattern of the movement, ‘peristalsis’, can not be accepted.
4. Sooner or later after the removal of the loop there can, on raising the intraluminal pressure in a moderate degree, occur powerful contraction waves with a remarkably prolonged period. This kind of waves is characterized in that they are superimposed with small contractions which are nothing but pre-existing waves. Consequently the large waves are to be regarded as a summated effects of pre-existing waves, being produced as a result of deterioration of the preparation.
5. After cooling the intestinal loop or cocainizing the mucosa of the loop, the loop always responds with uncoordinated contractions to a rise of the intra luminal pressure. From this it may be said that, when the intestine is released from the control of the intramural ganglion cells, its contractions lack the coordination.
6. On the basis of the results obtained in the present experiment as well as the previous ones which are especially concerned with the function of the intramural ganglion cells a new hypothesis is postulated to explain how the strength as well as the direction of the waves of the small intestine can be regulated.

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Investigations into the influences of precursors, members, and inhibitors of the citric acid cycle upon the sleep patterns were carried out in the rabbit with chronically implanted electrodes. The effects of these substances were compared before and after the pre-collicular transection.
EMGs were recorded from m. trapezius-pars cervicalis and m. scutuloauricularis superior, EEGs from the frontal cortex, olfactory bulb, and dorsal hippocampus. Changes of the duration and latency of the firstly appeared signs of the paradoxical sleep (PS) after injection of such substances into the aural vein, were adopted as criteria of the facilitatory or inhibitory effects of the substances upon the PS. The results are as follows:
A. In the decerebrate animal: 1) the latency of 31-190sec. and the duration of 50-470sec. are characteristic of the PS evoked by administering glucose-(10-30mg), and lactic acid (1.0-2.0mg), and pyruvic acid (1.0-2.0mg). 2) administration of 0.8-3.0mg of the members of the tricarboxylic acid cycle evoked the PS with latency of 20-270sec. and duration of 30-470sec. 3) spontaneous paradoxical sleep phase was not observed for more than 4 hours after the administration of fluoroacetate (0, 4-1.0mg); for 2 hours or more after the administration of malonic acid (1.0-2.0mg). Even if by co-administration of the inhibitors together with the precursors or the members of tricarboxylic acid cycle in gram equivalent, the PS was blocked. 4) after administering the short chain fatty acids (from C₂ to C₆; 0.6-1.2mg), acetoacetate (1.0-2.0mg) or acetone (0.8-1.2mg) the PS appeared with latency of 21-345sec. and duration of 20-487sec. 5) injection of DPNH (0.7-0.9mg) exercised a marked facilitatory effect upon the evocation of PS with 20-75 seconds latency and 180-960 seconds duration, whereas DPN, TPN or TPNH had no marked facilitating effect, but not produced inhibitory effect. 6) 2, 4-dinitrophenol (0.5-1.5mg) and 2, 3-dimercaptopropanol (0.7-1.0mg) produced neither facilitatory nor inhibitory effect.
B. In the intact rabbit, after administration of such precursors and members of the tricarboxylic acid cycle and DPNH, the PS was evoked as in the precollicular animal. However, the latency was longer than in the pre-collicular animal, while the duration was shorter. The PS threshold to direct electrical. stimulation of the septum or the hypothalamus decreased by 40-70 per cent of the control after injection of these substances. No appreciable change in the total amount of PS episodes was revealed following administration of 2, 4-dinitrophenol (0.5-1.5mg) or 2, 3-dimercaptopropanol (0.7-1.0mg), but an increased amount of total PS for 4 hours after administration of the precursors and the members of tricarboxylic acid cycle, and such coenzyme in respiratory chain as DPNH was observed. On the other hand, the appearance of PS was blocked by administration of fluoroacetate (0.4-1.0 mg) or malonic acid (1.0-2.0mg) just as in the case of the supracollicular transected rabbit.
C. In the control experiments of the intact animal, 0.2-0.3ml. of distilled water or physiological saline was administered and the PS appeared after the injection with the lapse of 22min. 30sec. to 58min. 50sec. except for one case with 19min. 10sec. After the transection it took 8min. to 30min. before the PS appearance.

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1. Effects of acetylcholine and adrenaline on the aconitine-inducedfibrillation were studied with microelectrodes on the right atrium isolated from young rabbits.
2. In the proper atrial muscle, acetylcholine (10^-5-10^-4) inhibiteddramatically the fibrillation and restored well synchronized and rhythmicaldischarges of equal magnitude.
3. In the sinoatrial node, acetylcholine also showed an inhibitory action on the irregular activity, producing an increase in resting potential, a decrease in slope of diastolic depolarization and a consequent decrease in pace-maker rhythm.
4. Contrarily, atropine (10^-7) was found to facilitate the aconitine-induced atrial fibrillation. Thus, by repeating acetylcholine and atropine infusions alternately, the fibrillation was possible to start or stop several times.
5. Adrenaline (10^-6) promoted the aconitine-induced fibrillation, inconcequence of an acceleration of pace-maker rhythm, frequent shift in pace-maker site and/or a production of two or more ectopic pace-makers. In the proper atrial muscle effect of adrenaline was not impressive, although it enhanced the rate of discharge and its irregularity.
6. Conflicting observations on effects of acetylcholine or adrenaline specially between the two kinds of fibrillation induced one by aconitine and the other by acetylcholine plus electrical stimulation were discussed, and dual sites of action of each drug were pointed out.
Finally, it was estimated that the cause of fibrillation in primary importance is a facilitation of sodium conductance which elicites an acceleration of the pace-maker potential.

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It has been shown that there exist marked differences between dogs andrabbits in the mechanisms of the febrile and the leukocytic response to en do-toxin. In dogs the leukocytic response seemed to be mainly due to the trapping of neutrophiles in liver and their later release. In the leukocytotic phaseimmature granulocytic form did not predominate and the role played by the ndogenous leukocytosis-inducing factor demonstrated in rabbits was only aminor one. In the state of endotoxin tolerance, although the febrile responsebecame markedly reduced, the leukocytic response remained almost unaltered.Thus the endogenous pyrogen also observable in dogs showed no correlationto the leukopenic response. It was demonstrated that the endogenous pyrogenhas been liberated from the liver in response to endotoxin. It was heat-unstable and pseudoglobulin in nature. The prevention of the endotoxin feverin the tolerant state or by glucocorticoid pretreatment was shown to be theresult of suppression of the hepatic responses to endotoxin including theliberation of the hepatic pyrogen. It was not the result of suppression of thecentral responsiveness.

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To examine whether the ATP's used by us during the past few years.had been considerably contaminated with calcium, the myofibrillar ATPaseactivities obtained with the five lots of ATP's were compared with eachother. From the results obtained, it was considered that the ATP's used byus probably belonged to the slowly hydrolyzing ATP's.

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1. The relation between the KCl concentration (10mM to 210mM KCl) andthe relaxation of glycerol-extracted muscle fibers induced by various relaxingfactors was demonstrated.
2. At each KCl concentration, the relaxation of fibers varied at most 3-6%in the Dowex A-1-pretreated reaction mixture and it was also 5-9%, even inthe reaction mixture to which a sufficient amount of Dowex A-1 was directlyadded.
3. 0.05mM EDTA caused markedly the fibers to relax independently on the KCl concentration.
4. The relaxation of fibers induced by 0.05 mg of microsomes per ml wasremarkable at relatively low KCl concentration, especially at 70mM KCl.

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1. The rate of calcium uptake and the amount of calcium stored by skeletalmuscle microsomes were remarkably dependent on temperature in the presenceof oxalate, while they were scarcely affected by temperature in the absenceof oxalate. The activation energy in the presence and absence of oxalate wasabout 20, 000cal/mole and 4, 500cal/mole, respectively.
. The rate of calcium uptake increased with increasing the amount of micro-somes in the presence and absence of oxalate. However, the saturation timewas 2 minutes even in 1mg/ml of microsomes in the presence of oxalate.
3. The amount of calcium stored increased with increasing calcium concentration in the presence and absence of oxalate. However, the relationship of hem did not coincide with the theoretical dissociation curve.
4. The rate of calcium uptake in the presence of oxalate decreased withincreasing calcium concentration.

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1. In normal rats, plasma PB¹³¹I was maintained at the initial level or slightlyelevated during repeated blood collections under ether anesthesia, which wasarbitrarily called “maintenance of plasma PB¹³¹I”.
2. Maintenance of plasma PB¹³¹I was not related to increased TSH secretion, but seemed to be induced by multiple factors including indirect involvementof normally functioning pituitary gland.
3. Vasopressin preparation failed to induce an increased thyroid activity ofnormal rats, but suppressed it, as assessed by lack of maintenance of plasmaPB¹³¹I following injection of vasopressin.
4. The suppressive effect was induced by both Pitressin and synthetic lysinevasopressin. But the former was more potent than the latter.
5. Pitressin injection which caused a thyroidal suppression in normal ratsaugmented TSH action to increase plasma PB¹³¹I in hypophysectomized rats.

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