1. Employing toad's myelinated nerve fibres as material and TASAKI-FRANK'S method of action potential recording, examinations were made on the action potential of single nodes of Ranvier in NaCl-, LiCl-and mixed solution.
2. In pure NaCl or LiCl solution, the size of the action potential increases simply and similarly with concentration, while, in a mixed solution where NaCl concentration is fixed, a maximum appears in the size at a certain LiCl-concentration. The maximal value is incomprehensively large.
3. The threshold is higher and the spike duration somewhat prolonged in the neighbourhood of the maximum.
4. Positive after-potential was observed occasionally in normal ionic condition, and much more clearly in mixed solutions.
5. It was supposed that the mechanism of action potential production must be much more complicated than believed usually.
The author wishes to express her sincere gratitude to Prof. K. YAMAGIWA and Prof. M. ICOMKA for useful advices and constructive criticisms throughout the present study, and for their kind help in preparing the manuscript.

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The comparative studies are carried out on the motility of the normal, denervated and aganglionic THIRY-loops of dogs.
The records obtained on the isometric contraction reveal that as for the level of the diastolic pressure or the tonicity in the resting state the aganglionic loop is in the highest rank among others, the normal one in the lowest and the denervated one in the intermediate, whereas as for the pressure developed or the tension developed the ranks are reversed. These facts suggest that the normal intestine contracts far more efficiently than the intestine lacking in some of its nervous elements.

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1. The effects of morphine upon the motility of the aganglionic, denervated and normal THIRY-je j unal loops of unanesthetized dogs were studied.
a) The intravenous administration of the amount of morphine ranging from 0.001 to 1.2mg/kg always produced an abrupt rise of tone accompanied with the decrease in superimposed rhythmic contractions in their amplitude. The tone was then gradually decreased accompanied with the increase in rhythmic contractions in their amplitude.At this stage the undulation of both tone and rhythmic contractions almost entirely disappeared.
b) It may be concluded that morphine acts as an excitant to the intestinal muscle itself, since the drug can raise the motility of the aganglionic loop.
2. Morphine could raise the intestinal motility which was previously depressed by atropine as well as by hexarnethonium.
3. The intravenous administration of morphine produced a transitory retardation followed by acceleration in the flow of fluid through the intestinal segment.

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The activity and the route of the olfactory centrifugal nervous system were studied in toads, frogs and bullfrogs.
1. When an electrical pulse was applied onto the anterior part of the diencephalon, an electrical wave was induced in the olfactory bulb (E-wave). The function of this wave was studied in connection with the one (A-wave) induced in the olfactory bulb by stimulation of the olfactory epithelium or nerve.
2. The E-wave generally has a strong inhibitory effect upon the A-wave which lasts for two to five seconds. This inhibition in the olfactory bulb was blocked by picrotoxin. On the other hand, the latter wave inhibits the former one only slightly and for 600 msec at the longest. Consequently, it was concluded that the inhibition of the A-wave by the E-wave is due to the real inhibitory mechanism, while that of the E-wave by the A-wave is due to the refractoriness of neurons in the bulb.
3. In a few cases, facilitation of the A-wave by the E-wave was found.
4. Similar inhibition was also found at various points of the cerebrum.
5. Recording of the E-waves at various points of the cerebrum surface disclosed that this olfactory centrifugal nervous system originates in the anterior part of the diencephalon, divides and courses as a pair of tracts along the lateral olfactory tracts bilaterally to the olfactory bulbs.
6. In the light of the histological finding, the neural mechanism of inhibition and facilitation was conceived in the olfactory bulb.The biological role of the centrifugal nervous system was considered.
The author is very much indebted to the Rockefeller Foundation for the contribution of some apparatus used in this experiment. Thanks are also due to Dr. H. FUJITA for his assistance in experiment and to Miss T. YAJIMA and Miss M. SARA-MOTO for for the preparation of figures. This work was carried out with the aid of a grant for scientific research from the Ministry of Education.

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1. Single spinal motoneurons of the cat were stimulated with linearly increasing currents flowing through an intracellular micropipette, and the changeability of threshold-latency curve depending upon circumstantial conditions was proved on one and the same motoneuron.
2. In a motoneuron, the threshold of which was relatively constant in wide range of the current inclination under slight anesthetization, an additional administration of Nembutal increased the threshold to slowly rising current but changed hardly the rheobase and the resting membrane potential, so that the threshold-latency relation became to depict upwards convex curve.
3. Slight stretch of the innervating and/or synergistic muscle of a motoneuron lowered the threshold to slowly rising current without appreciable change of the rheobase and the resting membrane potential. Consequently, this procedure approximated the threshold-latency curve to a constant level. The same but weaker effect was often elicited also by stretch of the antagonistic muscle.
4. Higher amplified recording of the motoneuronal membrane potential revealed that such slight stretch of synergists or antagonists produced relatively pure EPSP's or IPSP's of less than 1-2mV, converging irregularly and asynchronously to the motoneuron.
5. A small rectangular current step superimposed to linearly increasing current, applied at the moment of hundreds of milliseconds after the onset of the latter current, had a marked triggering effect upon spike initiation of the motoneuron, therefore, fired it with a lower current intensity than that of linearly increasing current alone.
6. Influences of anesthetics and background synaptic bombardments upon the accommodative attitude of motoneurons were discussed in concern with the triggering effect.

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The action of intravenous injection of a series of omega-amino acids on the cat spinal cord was investigated with intracellular recordings and test monosynaptic reflexes. The action of the omega-amino acids of carbon length seven and eight was opposite to that of the shorter chain omega-amino acids, producing a facilitation in extensor monosynaptic reflexes and a decrease in flexor reflexes.The action of the longer chain omega-amino acids was similar-to that of the shorter chain omega-amino acids in the following three criteria:(1) the effects on spinal reflexes were absent in decerebrate cats and present in spinal preparations, (2) the effect on flexor monosynaptic responses was reduced following administration of strychnine and (3) the effect on flexor monosynaptic responses abolished in the presence of conditioning volleys of high threshold afferent fibers from extensor muscles.
GABA (C₄) produced depression of extensor motoneurons with an increase of the membrane potential and facilitation of flexor motoneurons with a decrease of the membrane potential. A long chain omega-amino acid (C₈) depolarized extensor motoneurons and hyperpolarized flexor motoneurons. Some polysynaptic potentials were changed by injection of GABA without appreciable change in monosynaptic EPSP and IPSP from antagonistic muscle afferent fibers. Some intemeurons were depressed and other interneurons were facilitated by GABA. Significant effects of GABA were not found in Renshaw cells. It was suggested that short chain omega-amino acids selectively depress a certain spinal interneurons, while longer omega-amino acids activate these same interneurons.
The authors wish to thank Mr. S. TAKAI for his technical assistance. The authors also wish to express their appreciations to Dr. C. C. HUNT and Dr. E. R. PERL for their suggestions and criticism while preparing the manuscript. The present study was aided by a grant from the ministry of education of Japan and a grant, GA BMR 5809, from the Rockefeller Foundation.

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1. The prompt rise in the blood level of ACTH provoked in rats by such mild stresses as paw stimulation of epinephrine injection was significantly blocked by pretreatment of the animals with a small dose of Pitressin, while that following unilateral adrenalectomy was moderately inhibited. Pitressin, however, failed to suppress the ACTH release following such severe stress as laparotomy or immobilization.
2. ACTH once released into the general circulation seems to be potentiated by pretreatment of the animals with Pitressin.
3. The inhibitory effect of Pitressin is due to vasopressin itself, and not to its contamination with other substances contained in posterior lobe extracts.
4. In chronically stressed rats, the prompt rise of blood ACTH level was not observed after paw stimulation or unilateral adrenalectomy.The sensitivity of the adrenal gland to exogenous ACTH remained unchanged in these rats.
5. Posterior-lobectomy abolished the adrenal response to epinephrine injection. The resting level of blood ACTH remained high 3-4 days after the removal of posterior pituitary gland. Paw stimulation did not produce further elevation of the level of blood ACTH in these rats.
The authors are indebted to Dr. A. BRODISH for his help in the performance of blood ACTH assay. We wish to thank Prof. V. DUVIGNEAUD for his generous gift of the synthetic lysine vasopressin employed in this experiment.This study was supported by U. S. P. H. S. Grant A-256

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ACTH releasing activities of epinephrine, acetylcholine, Pitressin, synthetic lysine vasopressin and Pitocin injected into the carotid artery of rat were studied.
Pitressin and synthetic lysine vasopressin possessed the strongest potencies.
The dose threshold of Pitressin to induce an appreciable ACTH release fell between 40 and 80mU per rat.
Pitressin incubated with a kidney homogenate lost its ACTH releasing activity.
The rise in blood ACTH level following an intracarotid injection of 5ug. epinephrine was not altered when 40mU of Pitressin was administered simultaneously.
The authors are indebted to Prof. VINCENT DUVIGNEALD for the synthetic lysine vasopressin employed in this experiment. This study was supported by U. S. P. H. S. grant A-256.

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The effects of such vasoactive materials as Pitressin, epinephrine, norepinephrine and histamine on the hypophyseal portal vessels of rats were observed in situ.
These materials tested have been shown not to directly influence the hypophyseal portal vessels. The portal vessels, however, seem to be easily influenced by hemodvnamic changes in the systemic circulation or in the arterial vessels supplying the primary plexus of hypophyseal portal system.
The inhibitory effect of a small dose of Pitressin upon the ACTH release followino mild stresses must be mediated by factors other than the effect of the hormone upon the hypophyseal portal vessels themselves.
This study was supported by U. S. P. H. S. Grant A-256.

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1. Recovery of the excitability of the terminal Purkinje fibers of the dog ventricle was studied by means of intracellular stimulation and recording of membrane potential.
2. The strength-interval curve for the cathodal stimulation was a uniform hyperboloid with a sharp inflection. Their course was closely related to the membrane repolarization, and the relative refractory period corresponded to the phase of repolarization from-60 to-80mV.
3. The strength-interval curve for anodal stimulation had a shape of an inverted spike located about 15 to 20 mSec.earlier than the end of the absolute refractory period to the cathodal stimulation.The intact fibers were unresponsive to any anodal stimulation during the diastolic phase.
4. Break of anodal current produced an isolated spike response during phase 2 and in the first half of phase 3, but the response did not conduct. At a somewhat later stage, the anodal stimulation produced a response consisting of a spike and slow potential. In this case the response was conductive.
5. In view of the excitability curve of a single fiber, it is concluded that the excitation elicited by the extracellular anodal stimulation in the diastolic phase may be due to the virtually cathodal effect of the current around the anode, and the ‘dip’ or some of the irregularities observed in the extracellular cathodal strength-interval curves may largely be ascribable to the virtually anodal effect of the stimulating cathode.
The expenses for this work were defrayed, in part, by a grant from the Ministry of Education.

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