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VHFテレビ受信用の小型単指向性アンテナを開発した.このアンテナは2本の放射素子を用い, ハイブリッド回路, 移相回路および整合回路を介して位相給電したものであり, VHFテレビ全帯域にわたって単方向の指向性を示すものである.また小型化しているが, その利得は-5～+2.5dB程度であり, E面指向性はVHFテレビオールバンド8素子アンテナと同等なので, 強・中電界では従来の八木アンテナに代って使用できる.

1. Four giant neurones, designated G-H cells, in the right pleural ganglion of the marine pulmonate mollusc, Onchidium verruculatum, showed characteristic membrane hyperpolarization during applications of either acetylcholine (ACh) or L-glutamate. In the presence of ACh the membrane was hyperpolarized only transiently, while in the presence of glutamate the response was maintained. Significant increases in membrane conductance accompanied the changes in membrane potential. 2. In excess potassium sea water, a slight hyperpolarization occurred when the normal concentration was increased between one- and twofold. However, depolarization usually occurred when the concentration was increased tenfold except on a few occasions when a slight but definite hyperpolarization occurred. These changes were all accompanied by a substantial increase in the membrane conductance. This hyperpolarization was in all probability the result of an increase in chloride ion permeability caused by the release of an ACh-like transmitter from depolarized presynaptic nerve terminals. 3. The reversal levels for glutamate- and ACh-induced hyperpolarization respectively were approximately — 20 and — 17 mV with respect to the resting membrane potential. 4. By changing the external ion composition, glutamate- and ACh-induced hyperpolarization were shown to be the result of an increased permeability of the subsynaptic membrane to potassium and chloride ions respectively. It appears therefore that inhibition in the same G—H cells can be activated by two different transmitter substances and that each of them activates a change in the membrane permeability to a different ion. 5. The relationship between the concentration of glutamate and the membrane conductance change was suggestive of two glutamate molecules reacting with a single receptor site.

An anodal pulse applied during the falling phase of an action potential, if weak, produces a slight enhancement of negativity of the falling phase, but if increased in amplitude produces a split of the action potential into an early and "delayed" response and finally, complete abolition of the falling phase. If the pulse amplitude is increased still more after abolition, a second response is elicited. The latency to this second response following abolition is shorter than the latency to the delayed response, and further increase of the applied pulse amplitude cannot abolish this second response. To obtain abolition of the delayed response it is necessary to apply a considerably stronger anodal pulse near the peak of the spike than later during the falling phase. The reverse is true to obtain the second response. The anodal pulse sufficient to produce anode break excitation during the action potential and elicit the second response is ineffective applied to a resting node membrane. It is postulated that: a) due to an effect of the action potential itself the membrane is being actively depolarized during the early falling phase of the spike and b) the excitability of the node membrane is actually retained both during and following an action potential in the so-called refractory period but requires "resetting" by a positive pulse in order for re-excitation to take place.

Spontaneous unit discharges (SUD) were recorded simultaneously from the VMH and lateral area (LH) of the hypothalamus in cats by glass capillary electrodes. Effects of ether anesthesia and electrical stimulation of the LH and VMH structures on the activity of the VMH and LH alone and the reciprocal relation between them were determined. Distributions of SUD frequencies and interspike intervals were determined, and after the stationarity of the time series had been established, auto and cross-correlation functions were calculated. Results on the intimate reciprocal relation between the VMH and LH fit the predictions of a stochastic model quite well and were also confirmed by changes in the EEG recorded from both hypothalamic regions in chronic twelve-hour food deprived animals.

The relations between the nodes of stimulating current and excitation were studied on frog nerve with special emphasis on anode break excitation. The threshold for anode break excitation was several times greater than cathode make threshold. Following an exceedingly strong anodal pulse, there is a period of marked reduction in anode break threshold. The data indicate that anode break excitation in whole nerve results from node membrane breakdown, as concluded in a previous investigation on the single Ranvier node. The many confusing results often obtained in demonstrating Pflüger's law on whole nerve were found to be attributable to populations of nerve fibers in whole nerve and are readily explained by the results of single-fiber experiments.

IT is generally accepted that the lateral hypothalamic area (LH) and ventromedial nucleus (VMH) have a reciprocal relationship in the control of feeding behaviour1–3, and that some neurones in these regions are sensitive to levels of glucose in the blood4,5 or to electro-osmotically applied glucose6. We have demonstrated that although about one-third of the VMH neurones increased their activity when glucose was applied, there are neurones in LH which are specifically inhibited by it. These neurones are activated by direct applications of insulin, 2-deoxy-D-glucose and 3-O-methyl-D-glucose7. Booth8 demonstrated that the injection of 1 µl of 5% D-glucose in the LH blocked insulin-induced eating. More recently Colin-Jones and Himsworth9 reported that an injection of 2-deoxy-D-glucose (2DG) into the LH causes a marked increase in gastric acid secretion and attributed it to the lack of metabolisable glucose in the LH neurones. The fact that the specific glucose-sensitive cells which are inhibited by glucose exist only in LH has been highlighted in a recent report in which gastric secretion induced by the peripheral administration of 2DG in the cat was blocked by specific and discrete lesions in the lateral hypothalamus10. Here we report that the inhibition of LH neurones induced by direct application of glucose is the result of membrane hyperpolarisation and possibly results from the activation of the sodium pump causing an increased extrusion of internal sodium.

INTRACELLULAR recording of cholinergic synapses in the Onchidium oesophageal ganglia revealed one neurone, V-3, in the visceral ganglion in which neither membrane potential nor conductance changes after perfusion with 0.5 mM acetylcholine. Significant depolarisation with increased membrane conductance was caused by 1.3 mM glycine. This response to glycine is opposite to that of the mammalian spinal motoneurone1–3. Neurones examined in the ganglia, except V-3, were not affected by glycine. Here we report the ionic mechanism of glycine depolarisation, and compare the effect of strychnine on glycine depolarisation with its antagonistic action of mammalian glycine inhibition4.

THE mammalian lateral hypothalamic area (LH) and the ventromedial hypothalamic nucleus (VMH) are involved in feeding and satiety function, respectively1. There is also reciprocity of electrical activity between the two2. Anatomically related to these areas, the amygdala has been shown to be involved in the same functions. Lesions of the basolateral nucleus of the amygdala results in hyperphagia3, while its electrical stimulation arrests feeding behaviour4. The stimulation of the amygdala also produces changes in the spontaneous discharge pattern of LH units, suggesting an inhibition or an activation–inhibition sequence between the LH and the amygdala5,6. We report here evidence that the inhibitory effect of the amygdala on the LH neurone is due to a long lasting inhibitory postsynaptic potential (IPSP) exerted through the stria terminalis.

THE lateral hypothalamic region (LH) is generally referred to as the feeding centre of the brain in the regulation of food intake, and many authors consider the ventromedial hypothalamic nucleus (VMH) to be the satiety centre1. Various hypotheses have been put forward to explain how the cells of these centres are activated, and one of these is the glucostat theory1. The existence of hypothalamic chemoreceptors, such as those sensitive to the concentration of blood glucose, can be inferred from studies of single unit discharges induced by intravenous or intracarotid administration of various solutions2–4 and from work on selective gold thioglucose lesions5. It has, however, been impossible to determine which centre is activated or inhibited first or whether both centres are modulated directly by a change in the concentration of blood glucose, because of the reciprocal relations which exist between the activities of the VMH and the LH2,6. We report here the direct effects of glucose on individual cells of the VMH and LH, which we studied by means of electro-osmotic applications of glucose from micropipettes—the method used by Krnjevic and Whittaker7 in other regions in the brain.

A transistorized high input impedance and low noise preamplifier which can be mounted on the electrode positioner in a chronic preparation for the recording of unit discharges is described.

A quantitative study of anodal break excitation in single frog nerve fibers has been carried out. An applied anodal pulse caused an increase in the critical level of depolarization for excitation. Anode break stimulation was effective only if the anodal pulse was immediately followed by depolarization of the single Ranvier node membrane. This condition can be obtained in three ways: 1) by applying the anodal pulse during a conditioning depolarization voltage, which must be equal to or greater than the threshold value for cathodal stimulation; 2) by applying a pulse of such large amplitude so as to produce membrane breakdown, which results in depolarization by intrinsic local currents; 3) by applying the pulse to a fiber already under the influence of intrinsic depolarization resulting from deterioration or high concentrations of potassium in the external solution. True anode break stimulation can only be produced by an exceedingly strong positive pulse. The membrane breakdown resulting from such a pulse, first reported by Stampfli in 1958, is discussed and a hypothesis is presented explaining the physiological implications of this phenomena.

Publisher Summary This chapter discusses the neuronal mechanism of feeding. Using rats and cats, researchers observed that the animals with bilateral lesions made by current passage through an extreme lateral part of the lateral hypothalamic area (LH) at the same rostrocaudal level as the ventromedial hypothalamic nucleus (HVM), showed aphagia (and adipsia) that finally ended in death, if gastric feeding was not applied, due to starvation in spite of the availability of food, and that bilateral lesions of the HVM produced hyperphagia and obesity supposed to be a release phenomenon from an inhibitory mechanism of the HVM. Striking control and modifications on electrical activities of the HVM and LH by the influence of the limbic system such as the amygdala (AM), septum, globus pallidus (GP) and mesencephalic tegmentum were also verified. Spontaneous unitary discharges (SUDs) in one center were decreased in number by repetitive electrical stimulation of the other center where the SUDs were increased. Moreover, using a statistical treatment of the time series of SUDs , we proved a significant negative cross-correlation between both centers.

SummaryThe response of the frog single nerve fiber immersed in Ringer solution containing excess potassium has been studied under a voltage clamp. Two clearly discernible inward ionic currents have been observed. These two currents have been associated with sodium and potassium respectively. The evidence presented strongly supports the presently accepted Ionic Theory of nerve activity.

Statistical treatment of recordings of spontaneous unit discharges from the ventromedial nucleus and the lateral area of the hypothalamus (the activities in one area being recorded while the other was stimulated) revealed significant reciprocal relations. The concept that glucose-sensitive neurons are present in the ventromedial nucleus was supported by the effects on the spontaneous unit discharges of injecting glucose and other-solutions intravenously.

A transistorized high input impedance, low noise and high stability preamplifier is described. The circuit has a wide linear dynamic input range. The circuit can be miniaturized for chronic preparations and the recording of unit discharges by placing the two relatively large potentiometers in a remote location.

A single and double microelectrode positioner for use in chronic preparations to record unit activity is described. A jig for the accurate positioning of the electrode and a push-pull hydraulic driving mechanism are also described.