Tatsunosuke Araki

Bio: Tatsunosuke Araki is an academic researcher from Kyoto University. The author has contributed to research in topics: Depolarization & Excitatory postsynaptic potential. The author has an hindex of 6, co-authored 11 publications receiving 515 citations.

Response of single motoneurons to direct stimulation in toad's spinal cord.

Abstract: THE ACTIVITIES of single nerve cells explored with intracellular electrodes have been reported by several authors (1, 3, 4, 14). In those reports researches whether were made in connection with orthodromic or antidromic. It the excitation via neural is desirable, however, to pathways, adopt the method of direct stimulation in order to get more detailed knowledge concerning the physiological properties of the soma membrane. Since the insertion out ordinarily without of microelectrodes into the visual control, there is no neurons must be carried possibility of having two separate microelectrodes lodging in the same neuron, the one for stimulation and the other for recording. The use of a twin-microelectrode was also found inappropriate for the present purpose, because of the electrical interference between each electrode due to their capacitative coupling. The only method available was therefore to use the same microelectrode with certain compensation circuits for both stimulation and recording. The results reported here were obtained with such a method on single spinal motoneurons of Japanese toads.

The electrical activities of single motoneurones in toad's spinal cord, recorded with intracellular electrodes.

Abstract: 1. By inserting glass micro-electrodes, whose external tip diameter was less than 1μ, into ventral horn cells in excised toad's spinal cord, the resting membrane potential and the action potential of single motoneurones were recorded.2. In response to a single stimulus delivered to a dorsal root, there appeared firstly synaptic potentials in a motoneurone, which brought about spike potentials when they attained a certain size by summation. Positive synaptic potentials were encountered occasionally.3. When stimulated antidromically by the impulses in ventral root fibers, the motoneurone responded with a slow negative potential which resembled the synaptic potential, followed by a spike potential of soma.4. The spike potential was followed by a negative after-potential and then by a positive after-potential whose relative size was much greater than that of the axon.5. Some motoneurones showed repetitive spike discharges for a short time immediately after the insertion of the micro-electrode. In these cases cyclic changes of the base-line potential were observed coincidentally with the period of spike discharge.6. Activities of cells which were supposed to be internuncial neurones were also recorded.7. The effects of constant currents flowing through motoneurones on the resting and action potentials were tested. It was found that the spike potentials were more sensitive to polarizing currents than synaptic and resting potentials.

Accommodation and local response in motoneurons of toad's spinal cord.

Abstract: 1. Electrical activities of single motoneurons in excised toad's spinal cord were explored with intracellular microelectrodes.2. On the oscilloscopic tracings, the initiation of spike potentials was classified into two types: an LR-type and an abrupt-type. It was shown that in the former spike potentials were initiated from the soma introduced by local response, while in the latter they were initiated from the initial segment of motor axon.3. Single motoneurons were stimulated by exponentially rising currents applied directly with intracellular electrodes and the threshold depolarization was investigated as a function of the latent time. The threshold depolarization remained unchanged while the latent time was less than about 10 msec. Beyond this limit, it rose gradually with increase in the latent time, showing accommodation of the motoneuron to sustained depolarization. Accommodation was more prominent in the initial segment of motor axon than in so ma.4. Hill's constant of accommodation λ was found ranging from 25.5 to 70 msec. in the initial segment.5. The local response was often observed in soma separated from the spike, with stimulating currents rising slow enough.6. Wedenski inhibition was proven to occur in the synaptic transmission to spinal motoneurons.7. Accommodation and local response in motoneurons were explained referring to the ionic hypothesis of excitation.

Excitatory synaptic actions between pairs of neighboring pyramidal tract cells in the motor cortex.

Abstract: 1. By spike-triggered averaging, we documented recurrent individual excitatory postsynaptic potentials (EPSPs) produced in 33 pyramidal tract (PT) cells (target) by the activity of axon collaterals...

Effects of electrotonus on the electrical activities of spinal motoneurons of the toad.

Abstract: 1. Using single intracellular microelectrodes in a bridge circuit, the effect of electrotonus on the activity of motoneurons was explored in excised spinal cords of toads.2. A linear relationship was found between the applied current and the changes of the membrane potential, usually within a range of ±2.5 × 10-9 A, which caused shifts of the membrane potential by ±6 to 8 mV. With stronger currents, the rectifying action of the membrane was usually observed.3. The overshoot of the spike antidromically evoked remained almost constant, either when the membrane was depolarized or hyperpolarized to a certain extent. Stronger such polarizations, however, brought about insufficient or over-compensation.4. The effects of electrotonus on the afterpotentials were studied with similar results to those known from other cells.5. The size of PSP's was reduced by depolarization and augmented within a certain range of hyperpolarization. Monosynaptic EPSP was ineffective in evoking motoneuron spikes in the normal state, but sometimes became effective when the membrane had been suitably depolarized.6. With the combined application of two long square pulses, the motoneurons were excited directly under various background polarizations. Depolarized motoneurons showed responses only with short latency and a rather constant threshold depolarization. On the contrary, hyperpolarized motoneurons responded even with long latencies, the spike arising from a level of depolarization which becomes markedly higher with an increase in the latent time. The accommodation of motoneurons is discussed in connection with these findings.

The excitatory synaptic action of climbing fibres on the Purkinje cells of the cerebellum.

Abstract: 1. A single climbing fibre makes an extraordinarily extensive synaptic contact with the dendrites of a Purkinje cell. Investigation of this synaptic mechanism in the cerebellum of the cat has been based on the discovery by Szentagothai & Rajkovits (1959) that the climbing fibres have their cells of origin in the contralateral inferior olive. 2. Stimulation in the accessory olive selectively excites fibres that have a powerful synaptic excitatory action on Purkinje cells in the contralateral vermis, evoking a repetitive spike discharge of 5-7 msec duration. Almost invariably this response had an all-or-nothing character. In every respect it corresponds with the synaptic action that is to be expected from climbing fibres. 3. Intracellular recording from Purkinje cells reveals that this climbing fibre stimulation evokes a large unitary depolarization with an initial spike and later partial spike responses superimposed on a sustained depolarization. 4. Typical climbing fibre responses can be excited, but in a much less selective manner, by stimulation of the olive-cerebellar pathway in the region of the fastigial nucleus, there being often a preceding antidromic spike potential of the Purkinje cell under observation. 5. Impaled Purkinje cells rapidly deteriorate with loss of all spike discharge, the climbing fibre response being then reduced to an excitatory post-synaptic potential. This potential shows that stimulation of the inferior olive may evoke two or more discharges at about 2 msec intervals in the same climbing fibre. The complexity of neuronal connexions in the inferior olive is also indicated by the considerable latency range in responses. 6. A further complication is that, with stimulation in the region of the fastigial nucleus, the initial direct climbing fibre response is often followed by a reflex discharge, presumably from the inferior olive, which resembles the responses produced by inferior olive stimulation in being often repetitive. 7. Typical climbing fibre responses have been evoked by peripheral nerve stimulation and frequently occur spontaneously. 8. An account is given of the way in which the responses evoked by climbing fibres in the individual Purkinje cells can account for the potential fields that an inferior olive stimulus evokes on the surface and through the depth of the cerebellar cortex. 9. By the application of currents through the recording intracellular electrode it has been possible to effect large changes in the excitatory post-synaptic potential produced by a climbing fibre, it being diminished and even reversed with depolarizing currents and greatly increased by hyperpolarizing currents.

Core Conductor Theory and Cable Properties of Neurons

Abstract: The sections in this article are: 1 Introduction 1.1 Core Conductor Concept 1.2 Perspective 1.3 Comment 1.4 Reviews and Monographs 2 Brief Historical Notes 2.1 Early Electrophysiology 2.2 Electrotonus 2.3 Passive Membrane Electrotonus 2.4 Passive Versus Active Membrane 2.5 Cable Theory 2.6 Core Conductor Concept 2.7 Core Conductor Theory 2.8 Estimation of Membrane Capacitance 2.9 Resting Membrane Resistivitiy 2.10 Passive Cable Parameters of Invertebrate Axons 2.11 Importance of Single Axon Preparations 2.12 Estimation of Parameters for Myelinated Axons 2.13 Space and Voltage Clamp 3 Dendritic Aspects of Neurons 3.1 Axon-Dendrite Contrast 3.2 Microelectrodes in Motoneurons 3.3 Theoretical Neuron Models and Parameters 3.4 Class of Trees Equivalent to Cylinders 3.5 Motoneuron Membrane Resistivity and Dendritic Dominance 3.6 Dendritic Electrotonic Length 3.7 Membrane Potential Transients and Time Constants 3.8 Spatiotemporal Effects with Dendritic Synapses 3.9 Excitatory Postsynaptic Potential Shape Index Loci 3.10 Comments on Extracellular Potentials 3.11 Additional Comments and References 4 Cable Equations Defined 4.1 Usual Cable Equation 4.2 Steady-state Cable Equations 4.3 Augmented Cable Equations 4.4 Comment: Cable Versus Wave Equation 4.5 Modified Cable Equation for Tapering Core 4.6 General Solution of Steady-state Cable Equation 4.7 Basic Transient Solutions of Cable Equation 4.8 Solutions Using Separation of Variables 4.9 Fundamental Solution for Instantaneous Point Charge 5 List of Symbols 6 Assumptions and Derivation of Cable Theory 6.1 One Dimensional in Space 6.2 Intracellular Core Resistance 6.3 Ohm's Law for Core Current 6.4 Conservation of Current 6.5 Relation of Membrane Current to Vi 6.6 Effect of Assuming Extracellular Isopotentiality 6.7 Passive Membrane Model 6.8 Resulting Cable Equation for Simple Case 6.9 Physical Meaning of Cable Equation Terms 6.10 Physical Meaning of τ 6.11 Physical Meaning of λ 6.12 Electrotonic Distance, Length, and Decrement 6.13 Effect of Placing Axon in Oil 6.14 Effect of Applied Current 6.15 Comment on Sign Conventions 6.16 Effect of Synaptic Membrane Conductance 6.17 Effect of Active Membrane Properties 7 Input Resistance and Steady Decrement with Distance 7.1 Note on Correspondence with Experiment 7.2 Cable of Semi-infinite Length 7.3 Comments about R∞, G∞, Core Current, and Input Current 7.4 Doubly Infinite Length 7.5 Case of Voltage Clamps at X1 and X2 7.6 Relations Between Axon Parameters 7.7 Finite Length: Effect of Boundary Condition at X= X1 7.8 Sealed End at X= X1: Case of B1 = 0 7.9 Voltage Clamp(V1 = 0) at X = X1: Case of B1 = ∞ 7.10 Semi-infinite Extension at X = X1: Case of B1 = 1 7.11 Input Conductance for Finite Length General Case 7.12 Branches at X = X1 7.13 Comment on Branching Equivalent to a Cylinder 7.14 Comment on Membrane Injury at X = X1 7.15 Comment on Steady Synaptic Input at X= X1 7.16 Case of Input to One Branch of Dendritic Neuron Model 8 Passive Membrane Potential Transients and Time Constants 8.1 Passive Decay Transients 8.2 Time Constant Ratios and Electrotonic Length 8.3 Effect of Large L and Infinite L 8.4 Transient Response to Applied Current Step, for Finite Length 8.5 Applied Current Step with L Large or Infinite 8.6 Voltage Clamp at X = 0, with Infinite L 8.7 Voltage Clamp with Finite Length 8.8 Transient Response to Current Injected at One Branch of Model 9 Relations Between Neuron Model Parameters 9.1 Input Resistance and Membrane Resistivity 9.2 Dendritic Tree Input Resistance and Membrane Resistivity 9.3 Results for Trees Equivalent to Cylinders 9.4 Result for Neuron Equivalent to Cylinder 9.5 Estimation of Motoneuron Parameters

The Peripheral Nervous System

Abstract: Section I-Peripheral Nerve.- 1 Peripheral Nerve Structure.- 1. Introduction.- 2. Histology and Development.- 3. The Axon.- 3.1. Filaments and Microtubules.- 3.2. Other Organelles and the Axolemma.- 4. Sheaths of Axons.- 4.1. Schwann Cells.- 4.2. Myelin.- 4.3. Function of Schwann Cells and Their Myelin Sheaths.- 4.4. Connective Tissue Sheaths.- 5. References.- 2 The Nerve Impulse.- 1. Introduction.- 2. Passive Electrical Properties.- 3. Voltage-Clamp Analysis of the Ionic Current.- 4. Momentary Current-Voltage Relations.- 5. The Threshold Conditions for Excitation.- 6. Factors Determining Conduction Velocity.- 7. References.- 3 Axoplasmic Transport-Energy Metabolism and Mechanism.- 1. Introduction.- 2. Fast Axoplasmic Transport.- 2.1. Characterization.- 2.2. Mechanism and Energy Supply.- 2.3. Transport and Membrane Function.- 3. Slow Axoplasmic Transport.- 3.1. Characterization.- 3.2. Mechanism.- 4. References.- Section IIA-Junctional Transmission-Structure.- 4 Neuromuscular Junctions and Electric Organs.- 1. Introduction.- 2. The Typical Neuromuscular Junction.- 2.1. Distribution and Location of Nerve Terminals.- 2.2. The Axon.- 2.3. The Synaptic Space.- 2.4. Postjunctional Muscle Fiber.- 3. Variations of Motor End Plates.- 3.1. Variations from Class to Class.- 3.2. Endings on Slow-Twitch and Rapid-Twitch Fibers.- 3.3. Endings on Slow Tonic Muscle Fibers.- 4. Electric Organs.- 4.1. Electrocytes.- 4.2. Innervation and Ultrastructure.- 5. References.- 5 The Peripheral Autonomic System.- 1. Anatomical Considerations: Sympathetic and Parasympathetic Divisions.- 2. Morphological Observations.- 2.1. Preganglionic Neurons.- 2.2. Postganglionic Neurons.- 2.3. Adrenal and Extra-Adrenal Chromaffin Cells.- 3. References.- 6 Ultrastructure of Ganglionic Junctions.- 1. General Considerations.- 2. Sympathetic Ganglia.- 2.1. Amphibia.- 2.2. Reptiles.- 2.3. Mammals.- 2.4. Some Effects of Different Fixatives.- 3. Parasympathetic Ganglia.- 3.1. Ciliary Ganglion.- 3.2. Otic Ganglion.- 3.3. Ganglia of the Enteric Plexuses.- 3.4. Cardiac Ganglion Cells.- 4. Summary and Comment.- 5. References.- Section IIB-Junctional Transmission-Function.- 7(i) Neuromuscular Transmission-Presynaptic Factors.- 1. Synthesis, Storage, and Release of Acetylcholine.- 1.1. Synthesis of ACh.- 1.2. Storage and Release.- 2. The Acceleration of Release by Nerve Impulses.- 2.1. The Role of the Nerve Impulse.- 2.2. The Role of Ca2+.- 2.3. After- Effects of Depolarization-Secretion Coupling.- 3. References.- 7 (ii) Neuromuscular Transmission-The Transmitter-Receptor Combination.- 1. Introduction.- 2. Molecular Basis of Chemoelectric Transduction.- 3. Pharmacology.- 4. Chemical Nature of the Acetylcholine Receptor.- 5. Desensitization.- 6. References.- 7 (iii) Neuromuscular Transmission-Enzymatic Destruction of Acetylcholine.- 1. Location and Measurement of Cholinesterases at the Junction.- 1.1. Histochemical Staining.- 1.2. Microchemical Methods.- 1.3. Assay of External AChE.- 1.4. Radioautographic Methods.- 2. Amounts and Types of Cholinesterase at the Junctions.- 3. Requirement for AChE in Impulse Transmission.- 4. Relation of AChE to ACh- Receptors.- 5. Quantitative Relation of AChE to ACh at the End Plate.- 6. References.- 8 Ganglionic Transmission.- 1. Introduction.- 2. Response of Autonomic Ganglia to Preganglionic Volleys.- 2.1. Response of Normal Ganglia.- 2.2. Response of Curarized Ganglia.- 2.3. Slow Ganglionic Responses and Afterdischarges.- 3. Electrical Constants of Ganglion Cell Membrane.- 4. Action Potentials of Single Ganglion Cells.- 4.1. Response to Antidromic Stimulation.- 4.2. Response to Direct Intracellular Stimulation.- 4.3. Response to Orthodromic Stimulation.- 4.4. Ionic Requirement for Generation of Action Potential.- 5. Nature and Electrogenesis of Postsynaptic Potentials.- 5.1. The "Fast" Excitatory Postsynaptic Potential.- 5.2. The "Slow" Excitatory Postsynaptic Potential.- 5.3. The "Late Slow" Excitatory Postsynaptic Potential.- 5.4. The "Slow" Inhibitory Postsynaptic Potential.- 6. Cholinergic and Adrenergic Receptors at Preganglionic Nerve Terminals.- 6.1. Cholinergic Receptor Site.- 6.2. Adrenergic Receptor Site.- 7. References.- 9 Function of Autonomic Ganglia.- 1. Introduction.- 2. Ganglia as Coordinating Centers.- 2.1. The Relay Hypothesis of Ganglionic Function.- 2.2. Development of a Stochastic Hypothesis.- 3. Experimental Evidence.- 3.1. Observed Patterns of Innervation.- 3.2. Ganglionic Activity and Factors Influencing It.- 3.3. Relative Autonomy of Ganglia.- 4. Conclusions.- 5. References.- 10 Peripheral Autonomic Transmission.- 1. Introduction.- 2. Definition of the Autonomic Neuromuscular Junction.- 2.1. Relation of Nerve Fibers to Muscle Effector Bundles.- 2.2. Relation of Nerve Fibers to Individual Smooth Muscle Cells.- 3. Adrenergic Transmission.- 3.1. Introduction.- 3.2. Structure of Adrenergic Neurons and Storage of Noradrenaline.- 3.3. Electrophysiology of Adrenergic Transmission.- 3.4. Ionic Basis of the Action of Catecholamines on the Postjunctional Membrane.- 3.5. Summary.- 4. Cholinergic Transmission.- 4.1. Introduction.- 4.2. Localization of Acetylcholinesterase.- 4.3. Electrophysiology of Cholinergic Transmission.- 4.4. Ionic Basis of the Action of ACh on the Postjunctional Membrane.- 4.5. Summary.- 5. Purinergic Transmission.- 5.1. Introduction.- 5.2. Electrophysiology of Purinergic Transmission.- 5.3. Summary.- 6. Conclusions.- 7. References.- 11 "Trophic" Functions.- 1. Introduction.- 2. Regulation of Taste Buds.- 3. Regulation of Amphibian Limb Regeneration.- 4. Regulation of Physiological and Metabolic Properties of Muscle.- 4.1. Resting Membrane Potential.- 4.2. Acetylcholine Sensitivity.- 4.3. Cholinesterase Activity.- 4.4. The Role of ACh Release.- 4.5. The Dynamic Nature of the Muscle Fiber.- 4.6. Plasticity of the Motor Unit.- 5. Mechanisms of Neural Regulation.- 6. References.- Section III-Receptors-Structure and Function.- 12 Cutaneous Receptors.- 1. Introduction.- 2. Morphology of Cutaneous Nerves.- 2.1. Uniformity of Cutaneous Axons.- 2.2. Relative Numbers of Myelinated and Nonmyelinated Axons.- 3. Morphology of Cutaneous Receptors.- 3.1. Encapsulated Receptors.- 3.2. Unencapsulated Corpuscular Receptors.- 3.3. Noncorpuscular Receptors.- 4. Physiology of Cutaneous Receptors.- 4.1. Cutaneous Mechanoreceptors.- 4.2. Cutaneous Thermoreceptors.- 4.3. Nociceptors.- 5. References.- 13 The Pacinian Corpuscle.- 1. Introduction.- 2. Morphology.- 3. Afferent Responses to Mechanical Stimuli.- 4. Mechanical Properties of the Corpuscle.- 5. Receptor Potentials.- 6. Impulse Activity in the Nerve Terminal.- 7. Distribution of Pacinian Corpuscles.- 8. Central Effects of Impulses from Pacinian Corpuscles.- 9. References.- 14 Receptors in Muscles and Joints.- 1. Introduction.- 2. Joint Receptors.- 3. Tendon Organs.- 4. Muscle Spindles.- 4.1. Reptiles.- 4.2. Amphibia.- 4.3. Birds.- 4.4. Mammals.- 5. Uncertain Origin of Adaptation.- 6. References.- 15 Enteroceptors.- 1. Introduction.- 2. Methods.- 2.1. Histology.- 2.2. Physiology.- 3. Cardiovascular Receptors.- 3.1. Systemic Arterial Baroreceptors.- 3.2. Pulmonary Arterial Baroreceptors.- 3.3. Ventricular Receptors.- 3.4. Atriovenous Receptors.- 4. Respiratory System Receptors.- 4.1. Cough and Irritant Receptors.- 4.2. Pulmonary Stretch Receptors.- 4.3. Type J Receptors.- 4.4. Other Receptors.- 5. Alimentary System Receptors.- 5.1. Muscular Receptors.- 5.2. Serosal Receptors.- 5.3. Muscularis Mucosae Receptors.- 5.4. Chemoreceptors.- 5.5 Hepatic Osmoreceptors.- 6. Urinary Tract Receptors.- 6.1. Bladder.- 6.2. Urethra.- 7. Other Enteroreceptors.- 8. References.- 16 Arterial Chemoreceptors.- 1. Introduction.- 2. Structure.- 2.1. Light Microscopy.- 2.2. Electron Microscopy.- 2.3. Degeneration Studies.- 3. Function.- 3.1. Types of Activity in the Nerve Supply to the Receptor Complex.- 3.2. The Type I Cell.- 4. The Identity of the Receptor.- 4.1. The Received View.- 4.2. A New Hypothesis.- 5. References.- 17 Taste Receptors.- 1. Introduction.- 2. Gustatory Nerve Fiber Response to Chemical Stimuli.- 2.1. Multiple Sensitivity of Single Chorda Tympani Fibers.- 2.2. Neural Code for Quality of Taste and "Across-Fiber Pattern" Theory.- 3. Electrical Responses of Gustatory Cells to Chemical Stimuli.- 3.1. Innervation and Structure of Taste Bud.- 3.2. How Do Gustatory Cells Respond to Chemical Stimuli?.- 4. References.

The action of γ-Aminobutyric acid on cortical neurones

Abstract: In cats under pentobarbitone anaesthesia, GABA was tested on cortical, pericruciate neurones and its action compared with IPSPs evoked by surface stimulation. GABA was applied to individual cells by microiontophoresis, while recording the membrane potential and resistance. When K citrate-recording electrodes were used, GABA always hyperpolarized the cell and lowered its resistance, like the synaptic inhibitory effect. By adequate polarization both the action of GABA and the IPSP could be reversed, at a similar level of membrane potential. Both could also be reversed by injecting Cl− into a cell from a KCl recording electrode and the new reversal potentials also did not differ significantly from each other: after this treatment, some cells could be excited with GABA. All these effects of GABA were only seen when it was applied outside the neurones; intracellular injections were ineffective. Since the reversal potentials for the action of GABA and the IPSP are approximately similar, it is concluded that GABA could be the main cortical inhibitory transmitter.