Ionic currents in excitation and effects of acetylcholine on them were examined with isolated young calf Purkinje fibers by means of the voltage clamp technique. It was found that in the control state the gNa, which increased markedly at the beginning of depolarization, decreased rapidly until about 50msec and thereafter slowly. The gK, which showed a marked decrease at the beginning of depolarization, showed a fairly rapid increase until 100msec and a gradual increase thereafter.
Acetylcholine showed no significant effects on the ionic current up to the concentration of 10^-6g/ml. In a concentration higher than 10^-5g/ml the gK decreased soon after the addition of acetylcholine, but increased later. The g_Na increased during the first phase of depolarization up to about 150msec, but beyond this phase it decreased progressively.

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A lot of evidence demonstrated in the normal adult, epileptic patient, unanesthetized but immobilized monkey and cat, that such brain masspotentials as electroencephalographic (EEG) and evoked potentials of man and animal show in relation to time, at least for the first approximation, properties of normal GAussian stochastic processes and this would suggest analogue bioinformations of the brain which functions as a statistical servosystem.

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With the aid of histochemical procedures developed by Falck and Hillarp, the lumber sympathetic ganglia and the toxic gland of the lower limb of the toad (Bufo vulgaris japonica) were examined.
1. Both SB and SC systems were considered to be adrenergic or catecholamine containing ones.
2. The toxic gland of the lower limb was supposed to be innervated by adrenergic nerve fibres originated from sB neurons in the sympathetic ganglia.
3. These nerve fibres which were supposed to innervate the toxic gland were assumed to innervate the smooth muscle-like cells surrounding the secretory cells of the toxic gland.
4. The function of chromaffin cells in the sympathetic ganglia was briefly discussed.

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The mechanisms of sensitization to the lethal effects of histamine induced by B. pertussis vaccine were found to be different from that induced by adrenalectomy. The frequent appearance of cardiac irregularities which occurred several minutes after the histamine injection was a characteristic feature in the vaccinated rats. In the vaccinated rats glucocorticoid did not afford a complete protection against the lethal effect of histamine; the cardiac irregularities remained unchanged. This is in contrast to the resuscitating effect of the corticoid in the adrenalectomized animals. For the induction of cardiac irregularities presence of both adrenal cortex and medulla were found to be necessary. The cardiac irregularities were not due to hyperkalemia.

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A digital computer input device has been developed for processing neurophysiological data in real time. It consists of two high speed electronic counters and two A-D converters. They make it possible to deal simultaneously with four different signals. Some examples of the application of this apparatus have been presented: a program for the high speed digitization of interspike intervals, simultaneous analog to digital conversion of EEG and spike frequency, cross-correlation functions between 2 spike trains and between the EEG and a spike train, finally, pre- and post-stimulus time histograms.

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On a papillary muscle and its corresponding false tendon from the dog heart, the transmembrane potentials of Purkinje and “transitional cells” were recorded.
The action potentials recorded along the surface of the false tendon had the shape, amplitude and rate of rise similar to those of the typical Purkinje fiber responses. The RMP of cells from the false tendon have also approximately the same value than that of Purkinje cells (FIGS. 2 and 3). When the exploring microelectrode reached the “terminal Purkinje” fibers their membrane characteristics decreased slightly. The magnitude of these differences was even greater when recording from transitional cells located within the junctional region (FIGS. 2f and 3f).
Variables of different nature were introduced in order to study the relationship between the rate of rise of action potentials from transitional cells and the propagation of impulses through the junctional region of Purkinje and myocardial cells. a) Progressive increase in the frequency of stimulation (FIGS. 4 and 5), b) diminution in external NaC1 (FIG. 6), c) lack of calcium (FIG. 10), d) anoxia (FIG. 8), e) low temperatures (FIG. 7). All these variables produced a decrease in the rate of rise and amplitude of the initial component of a transitional potential and consequently the propagation through the junctional region was delayed or blocked (FIG. 1).
Simultaneous recording from two transitional cells revealed that conduction velocity is slower in the junctional region than in the false tendon. This fact suggest that transitional potentials having a slow rate of rise and small amplitude may cause the delays or the blockages in propagation occurring in the junctional regions.

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The excised atrio-ventricular septum of a rabbit's heart and a papillary muscle and its attached false tendon from a dog's heart were used in order to study the effects of calcium deficiency on the propagation of impulses through the mammalian heart junctional regions. The preparations were isolated and perf used with aerated flowing Tyrode solutions. The transmembrane potentials of the different cardiac cells were recorded through conventional technics.
The perfusion with calcium-free solutions produced, within variable periods of time, a decrease in RMP, rate of rise and amplitude of action potentials. An increase in duration of the responses preceded the former changes. The sensitivity of the explored cardiac tissues to the lack of calcium varied, the Purkinje fiber response being the most modified (FIG. 1). All changes produced by calcium deficiency were reversible (FIG. 2).
The propagation of impulses through the A.V. node junctional regions was slowed and in some cases blocked (FIGS. 3, 4 and 5A). These effects were more evident and appeared earlier in the fibers joining the lower part of A.V. node and the bundle of His (N-H) than in the auricle-A.V. node junctional region (A-N). Similar effects were observed in the Purkinjemyocardial cells junction (FIG. 6) in which calcium deficiency changed in a greater proportion the propagation of the impulses travelling from Purkinje to myocardial fibers (P-M) than that in the opposite direction (M-P).
The changes in propagation were reverted by adding calcium either to the perfusing chamber or through a micropipette subjected to hydrostatic pressure and placed on the junctional region (FIGS. 5B, C and 7).
The results show that the outstanding effects of the calcium-free solutions on the junctional regions may be due mainly to modifications produced on the membranes of transitional cells generating “transitional potentials”. These modifications would be produced indirectly acting through the sodium ions carrying system.

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1. Analysis of electrolyte composition of human body sweat induced by simultaneous iontophoresis of noradrenaline and pilocarpine (noradrenaline sweating) revealed increased sodium and chloride concentrations as well as increased Na/K ratio, compared with the control sweating induced by pilocarpine alone.
2. Human body sweat induced by simultaneous iontophoresis of adrenaline and pilocarpine (adrenaline sweating) seems to present an increased sodium and chloride concentrations as well as increased Na/K ratio, while the difference from the control sweating is not statistically significant except for Na/K ratio.
3. On the basis of these findings on the human body sweat, and of the similar findings in the palmar sweat of the monkey, the alpha and beta adrenergic receptor mechanisms to control the sweat electrolyte concentration, was suggested to be present in the sweat gland of man as in the monkey.

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