The reactive hyperemia in dog's hind-limb in the resting state was examined. The methods used were mainly the constant volume perfusion and partly the constant pressure perfusion.
1. The magnitude of the reactive hyperemia was parallel to the length of occlusion time, while the maximal dilatation of artery was obtained after one minute occlusion. The duration of the reactive hyperemia was almost the same when the perfusion volume was above a certain level (26 ml/min) in the constant volume perfusion, and the perfusion pressure above a certain level (50 mmHg) in the constant pressure perfusion.
2. The inhibition of metabolism by use of IAc or FAc caused the disappearance of the reactive hyperemia and further the vasoconstriction after the release of occlusion. The acceleration of metabolism by uncoupling action of DNP caused the augmentation of the reactive hyperemia. The vascular responses of acetylcholine, bradykinin and adenosine were not changed by FAc treatment, while they were diminished, or even converted to vasoconstriction, by IAc treatment.
3. The different mediator substance will probably be released from the poisoned tissue by use of FAc and IAc when the metabolism is inhibited by these substances.

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With a strong flash from a xenon discharge lamp the electroretinogram (ERG) and retinal action potentials recorded by intraretinal lead were investigated.
1. The normal ERG of the frog consisted of an initial negative potential (the a-wave) and an initial positive potential (the b-wave) on which a series of oscillatory potentials was superimposed. The frequency of the oscillatory potentials was independent of the stimulus intensity used. With intensive illumination a notch was observed along the falling slope of the a-wave. Thus the a-wave in the frog's ERG seemed to develop two phases. The size of the late deflection (the late a-wave) usually surpassed that of the early one (the early a-wave).
2. Effects of metabolic inhibitors on the ERG were studied. When 1.0 mM iodoacetate-Ringer's solution was perfused through the eye -ball, the ERG including the oscillatory potentials was abolished in a relatively short time. The rhythm of the oscillatory potentials, however, was not affected by iodoacetate.
When 1.0 mM KCN-Ringer's solution or 1.0 mM azide-Ringer's solution was perfused through the eye-ball, the oscillatory potentials were slowed in the rhythm and depressed in amplitude from the end of the train. The late a-wave as well as the b-wave was found to be susceptible to KCN and azide. The a-wave withstood inhibitors-of cellular respiration. Anoxia also appeared to exert almost the same effect on the ERG components as respiratory inhi-bitors.
3. With the eye-cup preparations intraretinal recordings were obtained from retinal layers.
The bipolar cell layer was found to be the optimal site for recording the oscillatory potentials. Judging from this finding and the vulnerability of the oscillatory potentials to anoxia as well as respiratory inhibitors, the oscillatory potentials were tentatively assumed to originate in the bipolar cell layer primarily.
The depth-experiments in this study indicate that an origin of the early a-wave is located in the receptor layer, and that of the late a-wave in the bipolar cell layer behind the visual cells. Hence the early a-wave may be specified as the distal a-wave, and the late a-wave as the proximal a-wave.
The initial part of the deep response exhibited a rather complex mor phology: The deep electrode frequently detected a sharp positive potential appearing upon the proximal a-wave. This positive potential was proved to arise evidently after the notch which apparently segregates the a-wave into two components.
In the light of the present investigation, the duplex nature of the a-wave in the human ERG was discussed.

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1. Effects of synthetic lysine vasopressin on the plasma concentration of FFA and in vitro oxygen consumption of tissues were studied in the rat.
2. The plasma FFA concentration decreased significantly following the injection of vasopressin, while the effect of oxytocin was less marked. Pre-treatment with vasopressin caused a significant suppression on norepinephrine, effect in increasing the plasma FFA concentration.
3. In vitro oxygen consumption of liver slices and hemidiaphragms was related to the medium concentration of palmitate.
4. In vitro release of FFA by epididymal fat pads was not affected by the addition of vasopressin. FFA releasing effect of norepinephrine was not influenced by the presence of vasopressin.
5. In vitro oxygen consumption of brown adipose tissue, liver and diaphragm was significantly reduced by the addition of vasopressin into the incubation medium, while that of white adipose tissue was not affected by vasopressin.

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Extracellular recordings were made from single neurons in cat's ventrolateral nucleus (VL) of the thalamus to study the mode of their activity as relay neurons mediating cerebellar impulses to the cerebral cortex. The following results were obtained.
1. 144 VL units were recorded which fired with a short latency to brachium conjunctivum stimulation. Latencies ranged from 1.2 to 4.6 msec and the greatest number was between 1.5 and 2.0 msec. These units were presumably excited monosynaptically.
2. 68 out of 144 VL neurons could be driven antidromically by a stimulus to the pericruciate cortex. Lowest threshold points for the antidromic activation were predominantly distributed on the precruciate gyrus
3. Cortical stimulation also produced a prolonged inhibition of VL neurons, which may be attributed to recurrent inhibition. The inhibition was demonstrated after chronic ablation of the cortical gray matter.
4. 21 out of 144 VL neurons were activated synaptically by pericruciate cortex stimulation, suggesting the existence of corticofugal facilitatory projection to VL.
5. Globus pallidus and caudate nucleus stimulation usually had a facilitatory effect on VL neurons with occasional evoked discharges.
6. Stimulation of nonspecific thalamic nuclei produced discharges of VL neurons followed by a prolonged inhibition.
7. Functional relationships between VL relay neurons and the motor cortex were discussed and the role of VL neurons as the specific relay neuron was analized.

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1. The O₂ uptake by rhodopsin solution was demonstrated with the Warburg constant volume respirometer. The values of QO₂ of non-bleached and bleached rhodopsin were 12.56 and 2.52 respectively.
2. Following the addition of metal inhibitors it was demonstrated that the O₂ uptake by the rhodopsin solution might be attributed to the presence of nonheme iron in the solution.
3. It was demonstrated that no cytochrome oxidase activity was found in rhodopsin solution.
4. At the first stage, molecular oxygen was taken up by non-heme iron which might exist on the surface of the rhodopsin molecule. Then the oxygen was transferred to phospholipid which is a component of the rhodopsin molecule, so that the oxygen was not saturated for hours in vitro. 5. The non respiratory oxygen uptake by rod outer segments, reported in the previous paper, might be attributable to the function of the rhodopsin molecule.

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In the present study the factors which influence the critical level of membrane potential for the spike were investigated.
1. The relation between critical level and resting membrane potential was approximately linear, their average values were 50.5±6.9 mV (S. D.) and 82.9 ± 7.0 mV (S. D.) respectively and the correlation coefficient between them was 0.75. The critical level was independent of the time necessary to reach it. 2. When the membrane potential was changed artificially, the critical level was linearly related to the membrane potential up to 95 mV, above which the critical level showed a tendency to flatten off.
3. The critical level was observed to tend gradually towards the lower value as the external potassium was raised in either case the membrane potential was changed with the change of potassium concentration or maintained at the initial level.
4. The resting potential was little influenced by the external sodium concentration and the critical level was also almost constant until 50 mM, below which it showed a tendency to decrease.
5. It is concluded that the critical level depends on the membrane potential and the external potassium concentration but not on the sodium concentration of the external fluid.

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1. The resting potential of frogsartorius muscle fibers was determined by m.eans of a compensating method using two micro-electrodes and a current sensitive galvanometer as a null instrument.
2. The mean value of resting potentials immediately after the insertion of the micro-electrode was 86.87±8.28 mV (S. D.)
3. The changes in the resting potential were observed for four hours and it was found that the resting potential was maintained for four hours although it was accompanied by some irregular fluctuaton.
4. From thirteen potentiometric measurements within four hours, the mean resting potential of a fiber was calculated. The value ranged from 72.82 mV to 100.60 mV for ten different fibers and the average value was 88.84±8.35 mV (S. D.).

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1. Acid phosphatase activity was determined biochemically in various phases of secretory activity in the rat pituitary, median eminence and anterior hypothalamus.
2. Following dehydration acid phosphatase activity increased significantly in the posterior pituitary, but no change was demonstrable in other tissues studied. Pitressin administration caused a significant reduction of the enzyme activity in the posterior pituitary and anterior hypothalamus.
3. A marked elevation in the adenohypophysial acid phosphatase was observed after 7 and 14 days of exposure to cold respectively. A similar, though less significant increase in the enzyme activity was noted in the anterior hypothalamus after 7 days of cold exposure. Chronic exposure of animals to hot ambient temperature did not affect the enzyme activity in all tissues studied.
4. Thyroidectomy as well as administration of methylthiouracil brought about a significant elevation of the phosphatase activity in the adenohypophysis. Thyroxine treatment, on the other hand, failed to affect significantly the enzyme activity.
5. Gonadectomy caused a marked enhancement of the adenohypophysial acid phosphatase, while the enzyme activity was not affected by testosterone administration.
6. Adrenalectomy did not influence the acid phosphatase activity in the anterior pituitary.

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Determination of the intracellular localization of acid phosphatase by use of differential centrifugation showed an even distribution of the enzyme activity among mitochondrial, microsomal and soluble fraction of the whole brain. Microsomal fractions from the adenohypophysis and anterior hypothalamus contained less portion of the total activity. It was found that the enzyme in the soluble fractions was more inhibited by formaldehyde and less by tartrate or fluoride as compared with that in other fractions. Acid phosphatase of the rat adenohypophysis was chromatographically separated into three and that of the anterior hypothalamus into two, major components of activity. Prolonged exposure of animals to moderate cold brought about an increase in per cent distribution of the first major component. From the similarity in the pattern of per cent inhibition by various inhibitors between of these chromatographic components and the fractions after differential centrifugation, a possibility was suggested that the acid phosphatase primarily related to the secretory activity may be separable as an independent peak in DEAESephadex column fractions.

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