The responses of single auditory neurons of the cat to relatively complex, time-varying stimuli, that is, FM, AM, and FM-AM sounds, along the auditory pathway were studied.
1) Directional sensitivity of neurons in response to either ascending or descending FM sound was found at the superior olive and it became more distinct at the higher auditory centers.
2) Some medial geniculate units responded only to a particular direction of FM sound and did not respond to pure tone at all.
3) Neurons in the upper levels of the auditory pathway can be characterized by the rate of frequency modulation. Three kinds of collicular neurons can be classified according to their FM directionalities and the rate of frequency modulation.
4) Directional sensitivity of neurons in response to either increasing or decreasing AM sound was found at the cochlear nerve, with increasing AM predominating. In general, at the higher auditory centers, the slow-adapting type neurons are predominantly sensitive to increasing AM sound, while the fast-adapting type neurons, in particular “on” type units, are predominantly sensitive to decreasing AM sound.
5) Neuronal excitability did not vary significantly with the rate of amplitude modulation for “on” type units, but it was lower for the slowadapting neurons when the rate of amplitude modulation was slowed down.
6) The neuronal responsiveness to each of four kinds of FM-AM sounds was investigated. In the lower levels of the auditory pathway, there were no significant differences in response to each of the FM-AM sounds, while in the higher levels the neurons responded mainly to a particular combination of FM-AM sound which can be determined by the response characteristics by examining the FM and AM sounds independently.
7) The possible mechanisms of neuronal FM and AM directionalities were considered on the basis of synaptic excitation and inhibition.

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Summary The discharges of cardiac and intestinal sympathetic efferent, ear skin temperature, arterial pressure, and heart rate were simultaneously recorded in anesthetized, immobilized, and artificially ventilated rabbits. The responses to hypoxia and hypercapnia of various degrees, to asphyxia, and to thermal stimulation of the spinal cord were observed. Cardiac sympathetic activity and as indirectly determined cutaneous sympathetic activity were reduced during moderate to severe hypoxia and during hypercapnia, whereas splanchnic activity increased. In states of extreme hypoxia or asphyxia (PaO₂ below 20-25 mm Hg) there was a generalized increase of cardiac and intestinal sympathetic activity. During spinal cord cooling cutaneous vasoconstriction was evoked, while cardiac and intestinal sympathetic activity decreased. During spinal cord heating the reverse response, i. e., reduction of vasoconstrictor tone in the skin and increase of cardiac and intestinal sympathetic activity, was elicited. Bilateral vagus transection did not change the patterns of regional differentiation of sympathetic efferents observed during changes of blood gas composition and central thermal stimulation. Comparison of the heart rate responses in non-vagotomized and vagotomized animals revealed that both vagal and sympathetic efferents contributed to the heart rate responses observed in the present investigation.

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1. A study was made to clarify the nature of the intramacular microphonic potentials of the sacculus of goldfish in comparison with the more common, negative microphonic potential which can be recorded from the saccular lumen. The intramacular microphonic potential was evoked as mostly positive deflections and at the same frequency as sound, while negative microphonic potential was evoked at twice the frequency of the sound.
2. A comparison was made of different types of microphonic potentials obtained from various depths of the macula. Effects of pressure changes applied to the fish's abdomen were also studied.
3. Studies on input-output function disclosed that the intramacular microphonic potential was sinusoidal in shape for a weak sound, but it deviated from sinusoidal when sound intensity increased, for its negative deflections were clipped. It was found that the negative microphonic potential could be recorded only for such a relatively strong sound.
4. From these results, it was concluded that the intramacular microphonic potential represents the activity of hair cells of a homogeneous group. The operational characteristics of hair cell activity were drawn based on results of input-output studies.
5. The recording conditions of intramacular microphonic potentials are discussed in relation to the functional differentiation of the saccular macula whose dorsal and ventral halves are concerned only with the reception of compression and rarefaction phases of sound, respectively.

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1. Synaptic transmission from hair cells to afferent eighth nerve fibers was studied in goldfish's sacculus (inner ear) by recording the microphonic potential and excitatory postsynaptic potentials (EPSPs) simultaneously. The microphonic potential was recorded extracellularly from the base of hair cells, and EPSPs were recorded intracellularly from individual nerve fibers.
2. There was an excellent one to one correspondence between microphonic deflections and EPSPs. An EPSP followed each microphonic deflection with a delay of about 0.5 msec. The delay was found to stay unchanged for different frequencies of sound.
3. Spontaneous miniature EPSPs were observed. Duration of these miniature potentials, about 0.5 msec at their half-width, roughly coincided with the duration of the sound-evoked EPSPs. A close correlation was found between the duration of a microphonic deflection and that of the corresponding EPSP.
4. The EPSP changed in size when the membrane at individual afferent nerve terminals was polarized by a flow of extrinsic current. A hyperpolarizing current produced an augmentation of the EPSP, while a depolarizing current produced its diminution. The EPSP was reversed in sign when a strong depolarizing current was applied.
5. These results conform to the view that the transmission from hair cells to afferent nerves is chemically mediated and that the depolarization of hair cells as represented by the positive deflection in the intramacular microphonic potential would trigger the release of the transmitter.

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1) Tension fall after termination of a depolarization was studied on the bullfrog atrial muscle under voltage clamp by the double glycerol-gap technique.
2) The tension fall was composed of three different phases:(a) initial retardation, (b) principal rapid relaxation, and (c) final slow relaxation.
3) The initial and second phases appeared exponential with time after repolarization. At 17°C, the time constant of the former was 0.07-0.08sec and that of the latter, 0.3-0.4sec for 25 to 80mV depolarizations.
4) The tension and the rate of tension fall during the second principal phase appeared almost proportional to the maximal tension at the end of depolarization, and strongly depended on the membrane potential levels before and after repolarization.
5) The principal tension fall during relaxation at different potential levels was also exponential, and the time constant increased in a hyperbolic manner with depolarization.
6) The relationship between the logarithm of late tension around 1 sec after repolarization and the membrane potential level during relaxation was linear for the depolarizing side. For the hyperpolarizing side the tension, becoming independent of the potential, appeared as a mere function of time.
7) These results are discussed in connection with possibilities that the initial retardation of tension fall relates to probable Ca influx immediately after repolarization and the second principal phase of relaxation, to the Na-Ca exchange mechanism.

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1) Augmenting and recruiting responses in the sensory cortices were examined by means of laminar field potential analysis in the cortices. These responses were characterized and interpreted as follows: Augmenting responses are a deep thalamocortical (T-C) response followed by a superficial T-C response and recruiting responses are a pure form of superficial T-C response, deep and superficial T-C responses being two elementary components constituting various cortical responses induced by thalamic stimulation (see SASAKI et al., 1970).
2) Long-latency surface-negative potentials elicited in the somatosensory cortex (posterior sigmoid gyrus) by repetitive stimulation of the intralaminar thalamic nuclei were not due to recruiting responses actually generated in this area but attributable to the responses evoked in the underlying hidden cortex. Similar situations to those in the somatosensory cortex hold for “recruiting responses” recorded on the surface of the visual and auditory areas, i. e., the responses in the lateral and the ectosylvian gyri were assignable to activities generated in the underlying or neighboring hidden cortex.
3) Repetitive stimulation of the thalamic sensory relay nuclei given at a low frequency failed to evoke the augmenting response in the respective cortical sensory areas. It induced in some cases incremental responses in the sensory areas of the cortex; the depth profiles in the cortex were not in accord with the characteristic feature of the augmenting response in the anterior sigmoid gyrus.
4) The absence of superficial T-C responses in the form of recruiting responses as well as a component of augmenting responses in the sensory cortices suggests that there is little or no thalamocortical projection system for the superficial T-C response ending in these cortices.

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Changes in the membrane potential and spike frequency of the smooth muscle cells of the guinea pig urinary bladder in various ionic environments at normal and low temperature were investigated with the microelectrode method.
1) At 36°C the membrane potential was -37mV, and at 12.5°C it was -28 mV. The maximum slope of the membrane potential changes against logarithmically plotted [K]_o was steeper at 36°C (31mV per tenfbld change of [K]_o) than at 12.5°C (24mV).
2) When [K]_o was reduced to below 5.9mM, the membrane was depolarized at 36°C, although at low temperature (12.5°C) the membrane was slightly hyperpolarized.
3) At normal temperature, K-free solution, Na-free solution, and ouabain (10^-6g/ml) depolarized the membrane, and during the recovery after treatment with the above agents the membrane was transiently hyperpolarized up to -65mV.
4) The hyperpolarization during the recovery process was not produced in the Na-free solution and at low temperature (13°C).
5) In Cl-deficient Krebs solution, the membrane was transiently depolarized; then the control resting membrane potential level was restored. On replacement of Cl-deficient solution with Krebs solution, the membrane was transiently hyperpolarized. On replacement of ouabaincontaining K-free Krebs solution with Cl-deficient solution, the membrane was markedly hyperpolarized compared with replacement with Krebs solution.
6) The spike frequency was markedly modified in various ionic environments, i. e., depolarization of the membrane in Na-free, K-free, and ouabain-containing Krebs solutions caused increase of the spike frequency. During the hyperpolarization of the membrane, presumed to be due to activation of an electrogenic Na-pump, and at low temperature (10°C) spike generation was suppressed.
7) The ionic mechanism involved in the membrane potential of the urinary bladders is discussed in relation to the electrodiffusion potential and the electrogenic sodium pump.

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