A new rapid potential with a very short latency was reported in the human electroretinogram (ERG). This new potential was tentatively called the early potential (EP). The present experiment gave evidence that the EP in man is essentially identical with the early receptor potential (ERP) in other vertebrates. Intense photic stimulation with a very short rise time was needed to evoke the ERP in man.
1) The EP obtained from normal subjects was seemingly biphasic in form, consisting of a small cornea-positive phase followed by a dominant cornea-negative one. The latency of the cornea-positive phase was less than 30μsec.
2) The latency of the a-wave elicited with the intense stimulus was as short as 1.7 msec, being the shortest value thus far reported for the a-wave of the human ERG. This may support the view that an origin of the a-wave of the human ERG lies in the visual cells.
3) The amplitude of the cornea-negative phase of the EP in man was approximately linearly related to the stimulus intensity for the first 1.1 log units above the threshold. In this range of stimulus intensity, the a-and bwaves showed no significant increase in amplitude.
4) The EP in man was not so greatly affected by moderate light adaptation as the ordinary ERG components. This implies that at suitable levels of light adaptation the EP can be practically isolated from the ordinary ERG components.
5) The EP comparable in size and time course to the normal control was observed in long-standing simple atrophy of the optic nerve and complete obstruction of the central artery of the retina. The EP was entirely abolished in idiopathic total detachment of the retina as well as even in early stages of the primary pigmentary degeneration of the retina. These findings may indicate that the EP in man is closely related to the activity of the visual cells.
6) A new cornea-positive potential, the summit of which appeared between the cornea-negative phase of the EP and the a-wave, was detected in cats, albino rats, pigeons and tortoises. This finding, coupled with the arguments in this paper, may advance a working hypothesis that the EP showsan additional cornea-positive phase in some conditions.

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1. The effects of alcohols and acetone on the neuromuscular junction of frog sartorius muscles were investigated by observing Ach potentials, e.p.p.s and m.e.p.p.s intracellularly.
2. The amplitude of e.p.p.s was increased in up to about 1.5% ethanol-Ringer's solution and was decreased in more concentrated ethanol. In about 1.5% or more concentrated ethanol, the neuromuscular transmission was blocked completely in a manner of “ all-or-none” reversibly.
3. The amplitude of Ach potentials was increased in up to about 1% ethanol and was decreased when the concentration of alcohol was over about 1%. The effects of methanol and acetone on Ach potentials were approximately the same as that of ethanol.
4. The amplitude of m.e.p.p.s was increased gradually in ethanol Ringer's solutions as the concentration of alcohol increased. Even in 3% ethanol in which the neuromuscular transmission was blocked completely, many large miniature discharges could be observed.
5. The frequency of m.e.p.p.s was increased dramatically in alcohol- and acetone-Ringer's solutions. It was about 9 times original in 3% methanol, about 13 times original in 2.5% ethanol, about 10 times original in 1.5% npropanol and about 6 times original in 2.5% acetone.
6. Ach potentials, e.p.p.s and m.e.p.p.s were prolonged markedly in alcoholand acetone-Ringer's solutions.
7. The effective resistance of the muscle membrane was decreased in ethanol- Ringer's solution. It was about 88% original in 3% ethanol.
8. Based on these results of the present experiments, the mechanisms of the neuromuscular transmission and the effects of alcohols and acetone on neuromuscular junction were discussed.

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Using both the conventional Warburg and the spectrophotometric method, the sites of action of ethylcarbamate (EC) and some other narcotics on malic dehydrogenase and the linked electron transport system in rat heart and brain homogenates and liver mitochondria, were studied. The results obtained were as follows:
1. The addition of EC (over 0.1M) caused inhibition of oxygen uptake in malate oxidation by a heart muscle homogenate in the presence of cytochrome c (CYT. C) or methylene blue. On addition of nicotinamide adenine dinucleotide (NAD) the inhibition in the presence of the latter decreased significantly.
2. Addition of EC caused inhibition of the reduction of CYT. C, 2, 6-dichlorophenol- indophenol and ferricyanide in malate oxidation in the presence of cyanide. On further addition of NAD the degree of these inhibitions decreased.
3. In the presence of cyanide, the reduction of CYT. C by NADH was inhibited by 51% with EC (0.3M), while in the absence of cyanide, the reduction was apparently enhanced owing to the inhibitory action of EC on the reoxidation of reduced CYT. C by oxygen.
4. In the presence of EC, the reduction rate of NAD in malate dehydrogenation increased, and oxidation of NADH by oxaloacetate was not inhibited.
5. Of the systems tested the inhibition of NADH oxidase activity (the oxidation of added NADH by oxygen) by EC was the largest (FIG. 4).
6. The oxidation of para-phenylenediamine (PPD) with added CYT. C in the heart, liver and brain preparations was inhibited by EC (0.3M) and chloretone (CL, 0.01M) by 40 to 50%, though in the liver and brain the inhibition was 10% or less than in the heart preparation, while amytal (0.005M) and veronal (0.04M) caused little or no inhibition. On the other hand, in the absence of added CYT. C all inhibitions decreased by about 40%.
7. The oxidation of ascorbic acid (VC) with added CYT. C was inhibited similarly by the narcotics, but the inhibitions were significantly lower than those of PPD oxidation.
8. The oxidations of added reduced CYT. C in the heart and liver preparations, like those of VC, were inhibited by EC.From these results, the mechanism of action of EC on malic dehydrogenase and the linked electron transport system was discussed in relation to CYT. C, leading to the following conclusions:
Narcotics, ethylcarbamate and chloretone, inhibit not only the cytochrome c reduction system, but also the cytochrome c oxidation system (cytochrome oxidase) of the electron transport system linked to malic dehydrogenase.

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The perfusion experiments were performed with dog's submaxillary gland and the mechanism of salivary secretion and the initiation of the secretory potential were studied by means of the microelectrode technique. Results obtained are as follows:
1. The intracellular potentials were very sensitive to changes of K⁺ concentration in the perfusate. When K⁺ was raised over 13mM/l, the secretory potential completely disappeared, while the secretion was still observed. Even when Cl^- in the perfusate was replaced completely by sulphate, the secretory potential remained pratically normal 15minutes after starting the perfusion, but the rate of salivary flow decreased.
Therefore, the secretory potential is not the causal factor of secretion, and it seems to originate from some other factor than the Cl^- pump along the cell membrane of the gland acinus.
2. From the balance study, it was concluded that the gland lost K+ with the rate of about 14&Eq/g.gland/min. into the blood and saliva during the secretion, while it was restored into the gland from the blood after cessation of stimulation and the restoration was completed in 15min., Na⁺ and Cl^- were retained in thegland tissue en route from the blood to saliva by stimulation, while they werecompletely driven out and then into the blood during the restoration of 15min. By analysis of the ionic concentration in the gland tissue, a similar ionic movement was observed. The K⁺ in the gland decreased during the salivary secretion, whereas the Na⁺ concentration increased.
3. It is clarified by the aid of GOLDMAN'S equation that the rate of potassium permeability to that of the other ions increased more markedly in the secreting state than in the resting state. Thus, the equilibrium potential which ismanifested by the increase of K permeability during the stimulation of the gland seems to account for the hyperpolarization of the intracellular potential of the gland acinus. The secretion of saliva is not necessarily concomitant with the hyperpolarization of the cell membrane potential, and should be explained by some other factor than the secretory potential. A possible mechanism of salivary secretion was suggested in the discussion.

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Response patterns of the reflex potentials in the lumbar sympathetic trunk were analyzed repeatedly in 25 chloralose anesthetized cats, double shock stimulations as well as repetitive ones being delivered to either the sciatic or the radial nerve.
1. With a single shock stimulation of either nerve, two kinds of reflex potentials, the early reflex potential (ERP) of spinal origin and the late one (LRP) of supraspinal origin, were obtained in all the 21 animals of intact spinal cords examined. The ERP was observed more frequently by the sciatic nerve stimulation (76.2%) than by the radial nerve one (23.8%), although the LRP was obtained in all the 21 animals irrespective of the nerves under stimulation. Throughout this series of experiments, no appreciable difference was recognized between the sides of the nerves under stimulation.
2. As a result from double shock stimulations of either the sciatic or the radial nerve, the LRP showed significantly ealier recovery curves than the ERP in 5 animals of intact spinal cords examined, namely they appeared respectively at intervals of approximately 600 msec and 1.3 seconds and recovered completely at intervals of 2.2 and 2.5 seconds. It was noted that recovery curves of the ERP shifted markedly to the left side of those of the LRP and ERP noted above following spinal cord transection at the C₁ level, showing their minimum reflex responses at intervals of as short as approximately 150 msec and their complete recovery at those of about 1.4 seconds. No appreciable difference was observed between the nerves under stimulation including their sides. Mechanisms of these phenomena were discussed.
3. Repetitive stimulations of varied frequencies for 15 seconds were delivered to the sciatic nerve in 8 animals with intact spinal cords. Reduction of amplitudes of reflex responses except for dominant, initial responses were observed which recovered gradually at frequencies below 4/sec during the stimulation, although no reduction was recognized at frequency below 0.3/sec. With increase in frequency above 5/sec, reflex responses fused together to DC potential shifts of maximum 70μV with irregular waves on them during the stimulation, showing maximum values at frequencies from 10 to 50/sec.
Dominant, initial responses were observed throughout this series of experiments. It was also noted that depressions of spontaneous potentials lasted for 7 seconds after cessation of the stimulation, showing longer durations with increase in frequencies.
4. Response patterns of reflex potentials which were observed in 4 spinal animals likewise with repetitive stimulations of the sciatic nerve, were quite different from those in animals of intact spinal cords noted above, as was expected from the distinctly early recovery curve of the ERP in these spinal animals.
5. Results of unitary reflex discharges obtained in 6 animals of intact spinal cords with repetitive stimulations of varied frequencies of the sciatic nerve were compatible with those of reflex responses with repetitive stimulations noted above, showing marked, initial bursts of discharges following by pauses of discharges for 1-2 seconds and maximum discharges during the stimulation above 10 to 50/sec frequencies of stimulations.

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1. Studies have been made on the effect of tetrodotoxin for vasopressen release from the isolated pituitary gland of the rat and Ca movement in relation to the secretion.
2. The presence of tetrodotoxin in incubation media suppressed markedly (80%) the vasopressin release caused by the exposure of the gland to excess K solution. Such a suppression can also persist in Na-deficient media. ⁴⁵Ca movements of both efflux and influx under the exposing excess K are also suppressed by about 35%. However, apparent suppression by tetrodotoxin on vasopressin release and Ca movement were not seen at the resting state.
3. The potentiation of secretion caused by low temperature or the presence of SH reagent was not suppressed by tetrodotoxin.
4. The primary effect of tetrodotoxin is a suppression of the Ca movement in stimulus-secretion coupling, then secondarily the vasopressin output is suppressed.
5. The observations by electron microscope are considerably consistent with the experiment of vasopressin release.

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1. The slow depressive potential (SDP) has been investigated in the isolated frog retina deprived of the pigment epithelium. In this preparation, the SDP could be evoked easily by photic, mechanical or electrical stimulation with applying a 15mM Cl solution on the receptor side and of a Cl-free solution on the vitreous side.
2. The SDP was characterized as a biphasic transretinal dc potential change revealing the surface of the receptor side to be negative with respect to that of the vitreous side at first and then positive.
3. The SDP was definitely an ‘all-or-none’ response.
4. The SDP was elicited by a dc current across the retina when the electrode on the receptor side was positive.
5. Transretinal impedance decreased during the SDP, and the elevation in conductivity was of the order of 2-4 per cent.
6. The a- and b-wave was affected by the SDP. The b-wave abolished at the peak of the negative potential shift and it had the long recovery time The effect on the a-wave was not so remarkable as observed on b-wave and it restored its original amplitude when the negative potential shift returned to the original level.
7. Observations from this study suggested that an increase of extracellular volume caused by contractions of Müller cells and an increase of potassium ion concentration in the extracellular space could be expected during the SDP.

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1. The behavior of a neuron population of the LGN during a reversible retinal blockade achieved by application of high intraocular pressure was investigated in cats prepared with a midpontine pretrigeminal transection. All experiments were carried out in the dark-adapted state.
2. Upon retinal blockade, the postsynaptic component of the population response of the LGN increased in amplitude, while the presynaptic component of the response remained unchanged or showed a small increase in amplitude.
3. In the control animal, the recovery cycle of the postsynaptic component of the geniculate population response did not show a prolonged depressive phase, whereas the depressive phase became apparent during retinal blockade.
4. The after-positivity of the population response of the LGN also became conspicuous during retinal blockade.
5. The excitability of the terminals of the optic tract fibers of the LGN remained unaltered or showed only a small change during retinal blockade.

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1. Effects of massive AC stimulation on the activity of bullfrog heart were investigated and comparisons in the effects were made among the whole heart and the isolated strips of various portions. Dependency of the responses on frequency of the AC stimulation was also studied.
2. General effects of mass stimulation were observed to be divided into immediate and after-effects. The latter was further subdivided into after-inhibition and after-acceleration of augmentation.
3. The effects on the whole heart were considerably different depending on the position of electrode and on the voltage of stimulation. High voltages to the sinus venosus produced dominantly a negative chronotropic effect while those to the ventricle caused a negative inotropic effect. The atrial stimulation produced an intermediate response. Low voltage of stimulation elicited mainly the after-augmentation in every portion.
4. Isolated strips of the sinus, venosus, atrium and ventricle hehaved quite similar in the responses to those of the sinus, atrial and ventricular stimulation of the whole heart respectively. Only exception was a slenderness of after-augmentation in the isolated sinus.
5. In the sinus venosus in situ, indirect stimulation of the vagosympathetic nerve produced almost the same effects to those of direct mass stimulationc applied on the sinus. The sustained contraction, however, was never produced by indirect nerve stimulation.
6. Increase in frequency of AC stimulation produced a decrease of the immediate- and after-effects. Low frequencies elicited a marked sustained contraction and an after-inhibition followed by a long lasting augmentation while high frequencies produced a fast but temporal augmentation. Thus, the frequency dependent changes appeared similar to the voltage dependent changes in such a way that high frequencies corresponded to low voltages and vice versa.
7. In all cases of the isolated strips and whole heart examined, the inhibitory after-effect was strengthened by ACh and completely blocked by atropine. The secondary after-effect of augmentation was depressed by adrenergic blockers such as inderal and reserpine.
8. These results suggest that the mixed electro-release responses can occur in a wide range of frequency of stimulation and also in different portions of the heart, though the responses vary depending upon areal difference of the electro-release and of function of the tissues.

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