The orthodromic cortical response induced by the olfactory nerve stimulation was analysed by the depth recording and also the commissural and the antidromic stimulations. The following results were obtained;
1. The orthodromic cortical response (OCR) consists of two components: the initial potential and the slow potential, negative in sign, at the cortical surface. When recording in the external plexiform layer, the negative deep spike of 3-5 msec duration occurred, following by the slow potential. The latency is about 15 msec from the onset of the initial potential and remains constant throughout the external plexiform layer. The recovery process of deep spike is extremely slow, requiring 2 sec or more for full recovery. In the deeper layer, unit discharge appeared.
2. In the internal granular layer the commissural cortical response (CCR) consists of positive-negative slow potential having a long latency of 60 msec. The deep spike does not interact with the preceding CCR.
3. The antidromic stimulation induces the grouped spike discharges and slow potential in the depth recording. The both negative slow potentials of OCR and antidromic cortical response (ACR) are depressed by the commissural stimulation, but the deep spike of OCR and the grouped spikes of ACR do not interact with the commissural stimulation.
From the above findings, it seems likely that the deep spike is generated in the radially oriented secondary element, namely the apical dendrites of the mitral cell.

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1. Single unit analyses have been done in 180 cortical auditory neurons of cats anesthetized with barbiturate.
2. A new type of the response area was found besides the flat type and the sharp peak type. The neurons of this type had multi-peaks in their response area.
3. An example of the multi-peak type was shown, and its response area and pattern suggested the direct projection of afferent fibers from the neurons of the medial geniculate body.
4. The flat type had the longest mean latency, followed the multi-peak type, and the sharp peak type.
5. The type of the response area changed from the flat type to the multipeak tpe or sharp peak type after the depth of the neurons encountered in a penetration.
6. The neurons obtained from a vertical penetration had the same characteristic frequency, and were presumed to be in a functional vertical column which was determined by the best frequency.
7. Many types of the response areas were involved in the neurons of the same penetration, and an integrative mechanism of the frequency was consid ered to be the convergence from the sharp peak type to the flat type via multi-peak type.
8. The changes in response properties caused by the two-tone stimulation were studied. The effect was more conspicuous in facilitation rather than inhibition, and observed mainly in the neurons with the narrow response area.
9. Facilitation occurred even when the two stimulating sounds did not give a beat, and the effective frequency range of some neurons was three bands far apart from their characteristic frequencies.
10. The effect differed after the frequency and intensity relation of the two tones.
11. In some cortical cells, the on response underwent different changes from that of the off response.
12. The threshold values were lowered especially at the high threshold frequency range of the response areas, and a new peak appeared in the response areas.
13. This facilitatory effect caused by the two-tone stimulation suggests that the cortical cells were sensitive to the change in frequency and intensity of the tonal stimuli, which seemed to be related to the discrimination of the complex sound.

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The cortical EEGs of the freely behaving cats were analysed by the use of an automatic frequency analyser during the wakefulness-sleep cycle where the three states, arousal, light sleep and paradoxical phase of sleep (PP) were distinguished. The spectral characteristics during PP and those during light sleep were described taking the spectrum during arousal as reference.
1. EEGs during PP: The sensorimotor cortex showed typically an increase of the slow waves (1-12 c/sec) and the fast waves (30-60 c/sec). Mostly the EEG of the auditory cortex behaved similarly. A decrease of the EEG components in the intermediate frequencies was seen in the associative and visual cortices; it occurred in the 10-30 c/sec waves in the visual cortex and in the 14-30 c/sec waves in the associative cortex.
2. EEGs during light sleep: The sensorimotor and auditory cortical EEGs were enhanced in the entire range of frequency below 30 c/sec with a slight decrease in the components faster than 30 c/sec. The visual and associative cortices showed an increase of the wave components slower than 14 c/sec and a decrease of the components in the range of 20-30 c/sec. Their 30-60 c/sec waves did not show a consistent change.
3. It was suggested that the process of activation maintaining “activated” sleep is not complete as in arousal.

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1. In normal rats intraperitoneal as well as intravenous in jections of Pitressin and synthetic lysine vasopressin caused a prompt fall in the rectal temperature. Pitocin and Syntocinon had no effect on it.
2. Intracarotid infusion of 8.5 per cent sodium chloride and 2 M sucrose solutions resulted in a lowering of the rectal temperature in normal rats, but not in neurohypophysectomized ones. Intravenous infusion of the hypertonic solutions and intracarotid infusion of isotonic solutions did not cause any change in the rectal temperature.
3. Exposing neurohypophysectomized and totally hypophysectomized rats to a high ambient temperature of 40°C for 40 minutes resulted in a similar rise of the rectal temperature in extent and mode to that in normal ones. In rats with anterior hypothalamic lesions the rectal temperature rose to a higher level over 41°C on exposure to the same heat conditions.
4. Subcutaneous injection of Pitressin tannate in oil caused a prolonged fall in the rectal temperature, but it did not exhibit any suppressing effect on the elevation of rectal temperature either in normal or in neurohypophysectomized rats which were subjected to heat exposure.
5. No difference was observed between intracarotid and intravenous route of Pitressin administration in the extent and the time course of the fall in the rectal temperature.
6. The fall in the rectal temperature following intravenous infusion of Pitres-sin was not modified by electrolesions in the anterior hypothalamic area, neurohypophysectomy and total hypophysectomy.
7. Neither treatment with Dibenzylin nor atropine affected the body temper-ature lowering effect of Pitressin.

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1. The administration of synthetic lysine vasopressin (100 and 40 mU per 100g, i. p.) caused a marked decrease in the metabolic rate in fasted rats. Synthetic oxytocin (400 mU per 100g, i. p.) had no effect.
2. The administration of hypertonic sodium chloride solution (2ml per 100g, per os) caused a slight but significantdecrease in the metabolic rate in fasted rats. Chronic administration of 2 per cent sodium chloride solution for 7 days did not show any change in the metabolic rate.
3. In sugar administered rats the decrease in the oxygen consumption produced by vasopressin was associated with an elevation of the RQ. In rats with high RQ values exceeding 0.900 the suppressive effect of vasopressin was not observed.
4. The calorigenic effect of norepinephrine was entirely abolished by treatment with vasopressin.
5. In alloxan diabetic rats the suppressive effect of vasopressin was also observed, though the metabolic rate wasextremely low in these animals.
6. The results suggest that vasopressinexhibits its effect on the metabolic rate by suppressing fat utilization as metabolic fuel.

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1. By means of an electromagnetic flowmeter, the change in cardiac output in the carotid sinus reflex was studied in the dog.
2. A distinct decrease in cardiac output was observed on relatively wide elevation of the intrasinusal pressure.
3. This decrease in cardiac output was ascribable principally to inhibition of the sympathetic inotropic discharge to the heart.

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The P_O2-ventilation response curves in acute hypoxia, obtained by the rebreathing method in dogs, were determined in three series; hypocapnic hypoxia, normocapnic hypoxia and hypercapnic hypoxia. The alveolar P_o2, at maximum ventilation was taken as is critical point (C. P.) for the tolerance to hypoxia.
1. The average values of P_AO2 at C. P. were 19.9 (±3.49) mmHg during hypo capnic hypoxia, 23.6 (±3.97) mmHg during normocapnic hypoxia and 32.6 (±6.64) mmHg during hypercapnic hypoxia.
2. In spite of a marked difference in alveolar P_O2, arterial oxygen saturation at C. P. in hypocapnic hypoxia and hypercapnic hypoxia was of a similar magnitude, and remained at 20 to 25%(an average: 22.7%). It seems most probable that a depression of respiration does not occur as long as the arterial oxygen saturation is above 22.7%.
3. The author explained these differences in P_AO² at C. P. through the three series of experiments as due to the Bohr effect.

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In order to analyse the neuronal mechanisms of sympathetic nervous activities step by step from the periphery, response patterns of galvanic skin response (GSR) and photoelectric digital plethysmogram (PTG) were compared each other under various experimental conditions in 45 cats. For this purpose, direct responses of these two phenomena by stimulation of the ipsilateral preganglionic or postganglionic sympathetic nerves as well as reflex responses of these phenomena by stimulation of the contralateral sciatic nerve were recorded simultaneously in animals immobilized with Flaxedil. Acute as well as chronic spinal animals were used for the observation of the reflex responses.
1. In the case of GSR, distinct responses were observed even with single pulse stimulation of the preganglionic as well as of postganglionic nerves, whereas no response of PTG was obtained unless repetitive stimulation was employed. Furthermore, the response patterns of these two phenomena with repetitive stimulation were different with each other, the former showing the maximum height in the initial phase of the stimulation whereas the latter doing at about the end of the stimulation. These results may be attributable to the different characteristics of the effectors: the sweat gland and the skin blood vessel.
2. Reflex responses of GSR appeared even with single pulse stimulation in acute as well as in chronic spinal animals, whereas reflex responses of PTG did solely with repetitive one in either group of animals. Increase in amplitude of pulse waves of PTG was observed in association with rise of blood pressure in acute spinal animals in contrast to its decrease in chronic ones. Release from intensive tonic sympathetic impulses of the skin vessel following spinal transection may account for this result in acute spinal animals.
3. Frequency response curves of these phenomena differed according to the sites of stimulation of the preganglionic, postganglionic nerve and contralateral sciatic nerve, although no essential difference between the results of the two phenomena obtained by stimulation of each site of these nerves was observed. These differences may be respectively due to the specific characteristics of synaptic transmission in the sympathetic ganglia and also to the specific neuronal mechanisms of the spinal cord.
On the basis of these experimental results, it may be said that there is no essential difference between the neuronal mechanisms of GSR and PTG, so far as the spinal reflex mechanism and peripheral one are concerned.

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By using mercury-in-rubber strain gauge, mechanism of the increased finger volume during cold immersion was investigated on healthy subjects. Several minutes after cold immersion, finger volume increased as much as 2% of the initial volume. Average venous distensibility of the finger was smaller during CIVD of the finger in cold water than that of the finger in hot water. Average venous pressure of the finger in cold water (5°C) was 18.5 mmHg and that of the finger in hot water (40°C) was 9.2 mmHg. Capillary filtration coefficient of the finger in cold water was remarkably higher (.008ml/100ml tissue/min/mmHg) than that of the finger in hot water (.003ml/100ml tissue/min/mmHg). This is partly due to an increased number of the precapillary sphincters open to circulation by vasodilator metabolites and partly due to an increased porosity of the capillary membranes.
The increased finger volume is, therefore, explained by an accumulation of tissue fluid by 1) increasing capillary pressure because arteriolar vasodilatation during CIVD was not accompanied by a dilatation on the venous side, and 2) an increased outward filtration of the fluid from the capillaries due to an increased capillary surface area and porosity of the capillary membrane.

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