It has been demonstrated that the hyperglycemic response due to epinephrine secretion in anoxemia depends markedly upon the type of anoxemia induced. CO-anoxemia, a special type of anemic anoxemia, induced a marked one, whereas hypoxic anoxemia of considerable O₂ lack provoked only a slight one. The absence of chemoreceptor stimulation in the former might be responsible for this difference, since after extirpation of carotid bodies a marked hyperglycemic response was also observed in the latter case. It was concluded that the epinephrine secretion in anoxemia is conditioned by the anoxemic hypotension which is prevented by chemoreceptor stimulation, rather than the anoxemia itself.

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The anti-stimulant (Ach, 5-HT, nicotine, histamine) actions of GABA and its derivatives on the guinea-pig ileum were investigated.
1. The anti-Ach action of GABA was weak and variable. The stimulant effect of 5×10^-10-10^-9 mole/l Ach was reduced by 42% on the average of 11 experiments.
2. The anti-Ach action of N-methyl-GABA was about a tenth of that of GABA. N-Dimethyl-GABA produced hardly it an N-trimethyl-GABA had a synergestic action with Ach.
3. N-Acetyl-GABA had a slightly weaker anti-Ach action than N-methyl-GABA and N-phenyl-GABA had a far weaker one.
4. GABA-methylester and N-methyl-GABA-methyiester had not any anti-Ach action. N-methyl-GABA-butylester and N-methyl-GABA benzylester had a much stronger anti-Ach action than GABA. N-phenyl-GABA-methylester had a slightly stronger one.
5. In the anti-5-HT action of GABA, N-substitution by methyl-, phenyl-and acetyl-group decreased the activity more severely than in the anti-Ach action.
6. N-Methyl-GABA-butylester and N-methyl-GABA-benzylester were similar to GABA as the antagonist of 5-HT. N-Phenyl-GABA-methylester was somewhat inferior to GABA.
7. The anti-nicotine action of GABA was also decreased by N-substitution with methyl-, phenyl-and acetyl-group. But, the reduction of potency by these structural changes was far less than in the anti-Ach action.
8. N-Methyl-GABA-butylester and N-methyl-GABA-benzylester had a very stronger anti-nicotine action than GABA, while N-phenyl-GABA-methylester had a slightly higher potency.
9. In all the actions above mentioned, N-methyl-GABA-butylester was somewhat superior to N-methyl-GABA-benzylester.
10. In all the actions, the activity of GABOB was a half or a third of that of GABA.
11. Methylesters of nicotinic acid and isonicotinic acid had a stronger anti-Ach action or anti-5-HT action than the acids and their activity was about a tenth of that of GABA. Methyl nicotinate and methyl isonicotinate were superior to their acids in anti-nicotine action, too, and their activities was more powerful than GABA.
12. GABA had not any anti-histamine action, but N-methyl-GABA-butylester and N-methyl-GABA-benzylester had a considerably strong action.

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An investigation has been made to clarify the characteristics of somatic area II response to ipsilateral somatic I stimulation in cats. A typical response consists of a sequence of five similar surface-positive deflections (S, P1, P2, P3, P4) followed by a surface-negative deflection (D). The alterations of the response, which are induced by pentobarbital, include reduction or elimination of P3 and/or P4. When double shocks were delivered to somatic I, a surface-positive wave, not seen in the conditioning response, appeared at stimulus intervals of 20-190msec, and the surface-negative wave, which was longer in its peak latency than that of D of the conditioning response, became larger in amplitude at the same stimulus intervals. The positive wave was very susceptible to pentobarbital, while the greater amplitude of the negative wave was considerably resistant to this drug. However, the negative wave of the test response was blocked at longer stimulus intervals as the depth of anesthesia was increased. Mutual blocking effect between P3, P4, and the positive wave, which appeared by the test stimulus, and the postsynaptic surface-positive wave of afferent nerve origin was observed. It is suggested that the positive wave, not seen in the conditioning response, is caused by the facilitation induced by double shock stimulation, and that it is of similar origin to the postsynaptic positive wave of the primary response of afferent nerve origin. The facilitation is also considered to be caused by a multineuronal system.

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1. Two kinds of the intestinal intrinsic reflexes were investigated by recording the electrical activities of the denervated small intestine in the dog anesthetized with morphine and urethan. The electrical activities were recorded in most cases by means of the microelectrode inserted into the muscular coats and occasionally by an agar-agar-AgCl electrode.
2. When the mucosa is stimulated mechanically or chemically, the rate of the positive slow potentials and the number of the spike potentials superimposed on them increase above the stimulated spot, while below the stimulated spot the former increases slightly in rate, being accompanied by a diminution in amplitude, and the latter diminishes in number or disappears completely.
3. When the intestinal muscle is stimulated mechanically or chemically, both above and below the stimulated spot all the spike potentials disappear and the slow potentials decrease in amplitude, being accompanied by increase in rate.

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The olfactory bulb response to direct electrical stimulation was studied in succinylcholine-paralyzed rabbits. The following results were obtained.
1) The response set up by direct stimulation of the olfactory bulb is composed of two most stable components, i. e. spike and slow potentials. The response was compared with the findings of other investigators.
2) Regional difference of the response pattern is due to the thickness of the layer of olfactory nerve fibers. The spike is most prominent near the anterior portion of the bulb. In the hindmost portion, probably the accessory bulb, a complicated response was found.
3) Response amplitude-recording distance relation indicates that spike is rapidly decreased in amplitude, while slow potential does gradually. This depends mainly upon the lower threshold of slow potential than that of spike and also interglomerular transfer of activation.
4) Absolute and relative refractoriness of the spike was different from that of the slow potential. Absolute refractoriness of both potentials were respectively about 2 msec and 6 msec.
5) By means of the depth recording, element corresponding to the spike was discriminated from that generating the slow potential. It was found that the former is localized in superficial layer, while the latter in somewhat deeper one.
6) Gamma-aminobutyric acid and gamma-amino-beta-hydroxybutyric acid depressed the slow potential markedly while the spike remained unchanged. Close similarity of the slow potential to the cerebral dendritic potential was pointed out.
7) Procaine suppressed completely the spike, whereas the amplitude of slow potential was not markedly affected. Likewise strychnine abolished the spike but caused the slow potential to augment a little.
8) The spike and slow potentials were not significantly affected by curarine applied topically or intravenously.
The above evidences seem to offer further support for our hypothesis about origins of the spike and slow potentials: The former is due to the action potential of olfactory nerve fibers in the superficial layer, and the latter results largely from the activity of dendrites of mitral and tufted cells.

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1. In decerebrate and non-decerebrate cats the activity of the cardioregulatory and abdominal sympathetic nerves following venous infusion of saline solution was investigated by means of the action potential study.
2. The efferent impulses in the cardiac sympathetic nerve were inhibited by venous infusion. Such an effect was not abolished by cutting the sino-aortic nerves, but by cutting the vagi. Digital compression of the right or left atrial wall evoked a similar inhibition in the cardiac sympathetic nerve.
3. The efferent impulses in the cardiac vagal nerve were increased by venous infusion. Such a response was not abolished by cutting the sino-aortic nerves, but by cutting the contralateral vagus nerve.
4. The efferent impulses in the abdominal sympathetic nerves were inhibited by venous infusion. Such a response was not abolished by cutting the sino-aortic nerves, but by cutting the vagi.
5. From the results, it is concluded that the cardiac vagal afferent impulses following venous infusion cause an increase of the cardiac vagal tone and a diminution of the accelerator and vasomotor tones, thus the true reflex response following venous infusion may be bradycardia and hypotension. The result is contradictory to the BAINBRIDGE'S hypothesis. The cause of tachycardia, found by BAINBRIDGE, was discussed.

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1. The stimulating effectiveness of homologous series of alcohols, acetates and ethers were studied in the olfactory epithelium of the frog by successive and single application methods. The results obtained by both methods were entirely coincident.
The stimulating effectiveness of a saturated alcohol vapour increases following the increase of carbon number, but it decreases beyond C₆. The stimulating effectiveness of a saturated acetate vapour increases gradually as the carbon number increases. But that of ether vapour has a maximum at C₃, and it decreases as the carbon number increases.
2. The stimulating effectiveness of alcohol vapour from the aqueous solution was studied at the concentration of 0.001M and 0.01M. The results were different from those obtained by OTTOSON.
3. The stimulating effectiveness was studied in the homologous substances of equal thermodynamic activities. It was found that they are nearly the same when the value of the thermodynamic activity is 0.01, but that they become different when the value exceeds it. It was made clear that BRINK-POSTERNAK'S rule (1958) is only applicable in a small range of the values of the thermodynamic activity in the frog.
4. The stimulating effectiveness of alcohols was studied on the equimolecular basis. The results were coincident with the calculated values of the thermodynamic activities of these alcohols except at C₇ and C₈. The mechanism of such a deviation was considered.
5. The relation between the steric configuration of the odorous substance and the stimulating effectiveness was studied.
6. There were found a peak and a break in the curve which shows the stimulating effectiveness of homologous alcohols. The origins of these discontinuities were discussed.

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The properties of the olfactory bulb potential evoked by electrical stimulation of the olfactory mucosa were studied in rabbits immobilized with d-tubocurarine. The evoked potential was a slow negative wave when recorded from the surface of the bulb. In favorable conditions, the falling phase of the main deflection carried the second negative wave which was readily suppressed by barbiturate anesthesia and by the centrifugal impulses. The evoked potential reversed in polarity when the recording microelectrode was inserted in the deep layer. During high frequency stimulation of the anterior commissure the evoked potential was completely inhibited. The potential was suppressed by local application of gamma aminobutyric acid, Studying the unitary activity, it was observed that olfactory mucosa stimulation caused not only excitation but also inhibition of the single neuron discharge. These findings were discussed in relation to the histological structure of the olfactory bulb.

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1. Effects of systemic omega-amino acids on extensor and flexor monosynaptic reflexes were studied in unanaesthetized spinal cats.
2. Beta-alanine (C₃), delta-aminovaleric acid (C₅) and epsilon-aminocaproic acid (C₆) depressed the extensor monosynaptic reflex (EMR), while the flexor monosynaptic reflex (FMR) was usually facilitated. The potencies of C₃, C₅ and C₆ were 1/50, 1/30 and 1/70 respectively relative to that of GABA. Glycine (C₂) was ineffective.
3. The depressant action of these amino acids on EMR were inactivated by previous repetitive application of GABA.
4. Beta-alanine was ineffective on both EMR and FMR in decerebrate cats.
5. Omega-amniocaprylic acid (C₈) produced actions opposite to that of GABA, EMR being facilitated and FMR depressed. The potency of C₈ was 1/100 of GABA. The latency was longer than those of other amino acid actions, and the effect was not influenced by previous administration of GABA.

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The effects of interaction between cutaneous and cortically evoked motoneuron activities have been studied in cats. Cortical area stimulated was somatic sensorymotor areas I and II. Motoneuron activities were reflected in recordings from single nerve fibers to a contralateral forearm muscle. The forearm cutaneous nerve on the same side of the recording site was stimulated. The effects were that (i) the latency of the unit discharge became shorter or longer, (ii) the number of unit discharges increased or decreased, and (iii) these effects were mixed. The effects lasted for over 160msec. When cortical stimulation preceded, inhibition mostly occurred at shorter stimulus intervals (up to about 80 msec.) and facilitation, at longer stimulus intervals (over about 80 msec.). When cutaneous stimulation preceded, facilitation mostly occurred at shorter stimulus intervals and inhibition, at shorter and longer stimulus intervals. The preceding cutaneous stimulation dominantly produced facilitatory activities and cortical stimulation, inhibitory activties. The functional significance suggested is that cutaneous sensory information activates cortically induced motor acts which depress the cutaneous reflex.

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