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Biomedical subjects

K Koketsu

Publications and source records attributed to K Koketsu.

At least 91 records · Page 5Linked to original sources
PubMed1976

Adrenaline and the electrogenic sodium pump in Rana catesbeiana sympathetic ganglion cells.

The effect of adrenaline on the Na+-pump in bullfrog (Rana catesbeiana) sympathetic ganglion cells was studied by use of electrophysiological methods. The rate of removal of excess Na+ injected into a ganglion cell was increased by adrenaline. The K+-activated hyperpolarization of cell membrane, which might be produced by an electrogenic Na+-pump, was also increased by adrenaline. These results suggested that adrenaline was able to accelerate the Na+-pump, possibly the electrogenic Na+-pump.

Action Potentials↗
PubMed1976

Novel action of a piperazine derivative on the end-plate of the frog.

The effects of a piperazine derivative, trimetazidine (1-(2, 3, 4-trimethoxybenzyl) piperazine dihydrochloride) on the frog end-plate membrane were studied. Action and resting membrane potentials and the input resistance of muscle fibers were not affected by trimetazidine (82-165 muM). Under these conditions, the frequency of the miniature endplate potentials was unchanged while its amplitude was slightly decreased. The amplitude of acetylcholine (ACh) potentials were markedly and reversibly decreased after application of trimetazine (82-165 muM). The dose response curve of the end-plate membrane to ACh showed a non-competitive type of blockade. Trimetazidine (165 muM) not only decreased the amplitude of the end-plate currents (EPC) recorded from the glycerinated muscles using a voltage clamp technique, but also drastically shortened its time course. Under these conditions, the falling phase of the EPC became completely voltage insensitive. The equilibrium potential for the EPC slightly shifted to a more negative value in the presence of trimetazine (165 muM). Coefficient of variation of EPC was increased by Trimetazidine (165 mum), indicating a decrease in the quantal content of the EPC. The rate of desensitization of the end-plate to ACh was facilitated and the rate of decrease in EPC amplitude during tetanic stimulation became voltage sensitive by the action of trimetazidine (133 muM). It is concluded that trimetazidine mainly acts on the postsynaptic membrane with a weak presynaptic action. The agent seems to block a step subsequent to the interaction of ACh with its receptor, which presumably involves changes in the ion conductance of the membrane and is responsible for the voltage sensitivity of the response.

Acetylcholine↗
PubMed1976

The effect of adrenaline on the K+ -activated hyperpolarization of the sympathetic ganglion cell membrane in bullfrogs.

Effects of adrenaline on K+ -activated hyperpolarization of bullfrog sympathetic ganglion cells, preganglionic nerve axons and splanchnic nerve axons were studied. The K+ -activated hyperpolarization recorded from ganglion-postgangaline (0.3 mM). On the other hand, the K+ -activated hyperpolarization of postganglionic, preganglionic nerve axons and splanchnic nerve axons was not affected under the same experimental conditions. The facil-tatory effect of adrenaline on the K+ -activated hyperpolization was gradually intensified when the application of adrenaline was sustained for up to 60 min. The effect was reversible. The K+ -activated hyperpolarization recorded from ganglion cell-bodies by intracellular microelectrodes was similarly augmented by adrenaline (0.1 mM). Adrenaline in this concentration, however, caused no significant changes of the membrane potential and conductance in the presence of ouabain (0.002 mM) which completely and reversibly inhibited K+-activated hyperpolarization. Noradrenaline showed similar but less effected and isoproterenol showed no significant effect on the K+ -activated hyperpolarization. The facilitatory effect of adrenaline was inhibited in the presence of phentolamine but not of DCI. These results suggested that the intraganglionic membrane of ganglion cells possessed some kind of adrenergic alpha-receptors and the electrogenic Na+ pump of ganglion cells was accelerated by some unknown mechanism when adrenaline reacted to these receptors.

Animals↗
PubMed1976

The electrogenesis of adrenaline-hyperpolarization of sympathetic ganglion cells in bullfrogs.

Bullfrog sympathetic ganglion cells produced hyperpolarizing (Ad-hyperpolarization) and depolarizing (Ad-depolarization) responses when adrenaline (Ad) was directly applied to ganglia. The nature of Ad-hyperpolarization recorded by the sucrose-gap method was analysed in the present experiment, in order to clarify its electrogenesis. The amplitude of Ad-hyperpolarization was increased or decreased while ganglion cell membranes were hyperpolarized or depolarized, respectively, by applying a moderate conditioning current to the ganglia. The Ad-hyperpolarization was depressed in K+-rich solutions as well as in K+-deficient solutions. It was not significantly altered by replacing the extracellular total Cl ions by equimolar glutamate or thiosulfate ions. Ad-hyperpolarization was depressed and finally abolished in the Na+-free Tris solution, and was reversibly eliminated in the solution where Na ions were totally replaced by equimolar Li ions. It was enhanced when a preparation was previously perfused in the K+-free, Na+-rich solution for certain periods, during which the intracellular Na+ concentration might be increased. Ad-hyperpolarization was depressed by lowering the temperature and by the action of ouabain, and the amplitude of Ad-hyperpolarization was markedly increased in the presence of TEA. The ionic mechanism underlying the generation of Ad-hyperpolarization was discussed on the basis of these present experimental results, and it was suggested that Ad-hyperpolarization might be generated by an electrogenic sodium pump.

Acetylcholine↗
PubMed1976

Analysis of the slow excitatory postsynaptic potential in bullfrog sympathetic ganglion cells.

The ionic mechanism of the slow excitatory postsynaptic potential (slow EPSP), i.e. the muscarinic action of acetylcholine (ACh), was studied either by stimulating preganglionic nerves or by applying ACh in curarized sympathetic ganglion cells of bullfrogs. There are three different types of cells characterized by the effects of membrane hyperpoliarization on the amplitude of slow EPSP. One group of cells showed an increase in amplitude (type 1 cell) and, in two other groups of cells, it remained unchanged (type 2 cell) or decreased (type 3 cell), when the membrane was hyperpolarized. Under the muscarinic effects of ACh, the slope membrane conductance was increased (type 1 cell), unchanged (type 2 cell) or decreased (type 3 cell) at 10-20 mV hyperpolarized levels, while it was unchanged (type 1 cell) or decreased (types 2 and 3 cells) at resting and depolarized levels. In all cells, the slow ACh potential, corresponding to the slow EPSP, was almost completely suppressed in a high K+, Ca2+-free, Na+-free solution. These results suggest that the slow EPSP is generated by increases in Na+ and Ca2+ conductance and also by a simultaneous decrease in the K+ conductance.

Acetylcholine↗
PubMed1976

The muscarinic effects of acetylcholine on the action potential of bullfrog sympathetic ganglion cells.

The direct effects of acetylcholine (ACh) on Na+- or Ca2+-dependent action potentials of curarized sympathetic ganglion cells in bullfrogs were investigated under a condition where membrane depolarization caused by the muscarinic action of ACh was nullified by means of a hyperpolarizing current. ACh decreased the after-hyperpolarization of Na+-action potentials in Ringer's solution, and increased the after-depolarization of Ca2+-action potentials in the isotonic Ca2+ solution. In both solutions, the maximum rates of rise of the spikes were decreased and the slope membrane resistance at the original resting level was increased. The effects of ACh were abolished by atropine. On the other hand, ACh showed no significant effects on action potentials of bullfrog spinal ganglion cells which possessed no synapses. These results suggest that the ion conductance channels for generation of action potentials of sympathetic ganglion cells are under the direct control of transmitters, such as ACh.

Acetylcholine↗
PubMed1976

The actions of trimetazidine on nerve and muscle cells in frogs.

The effect of trimetazidine (TMZ) on cardiac, skeletal muscle fibres and sympathetic ganglion cells in frogs were studied. In cardiac muscles, the contraction was depressed and the duration of action potentials were shortened by 1.5 mM TMZ. In skeletal muscles, the contraction induced by motor nerve stimulations was depressed by 0.3 mM TMZ, and the amplitude of end-plate potentials was decreased under this condition. The nicotinic transmission in sympathetic ganglia was inhibited by 0.003 mM TMZ, but the muscarinic transmission was not affected by 1.5 mM TMZ. In a Na-free TEA solution, prolonged action potentials (TEA potentials) of sympathetic ganglion cell, which appeared to be produced by an inward Ca movement across the membrane, were shortened by 1.5 mM TMZ. These results suggest that TMZ has a dual action, namely 1) a blocking action of nicotinic transmissions and 2) a blocking action of Ca movement during the generation of action potentials.

Action Potentials↗
PubMed1975

Unusual cholinergic response of bullfrog sympathetic ganglion cells.

The membrane of bullfrog sympathetic ganglion cells was hyperpolarized by a direct action of ACh (more than 0.5 mM) in a solution containing both nicotine (0.24 mM) and atropine (0.14 mM). This ACh hyperpolarization could be imitated by neither carbachol nor bethanechol, suggesting that the ACh hyperpolarization was the response which was produced by a specific action of ACh, which appeared to be neither nicotinic nor muscarinic. The size of ACh hyperpolarization was increased during a conditioning hyperpolarization. The ACh hyperpolarization was completely blocked by ouabain (2 times 10(-3) mM) and eliminated in the Na-free lithium solution. These aspects of the ACh hyperpolarization suggested that generation of this hyperpolarization was associated with the sodium pump. The ACh hyperpolarization seemed to be partially responsible for the production of the slow IPSP, since a part of the slow IPSP remained occasionally in the presence of both nicotine and atropine.

Acetylcholine↗
PubMed1974

Effects of lithium ions on electrical activity in sympathetic ganglia of the bullfrog.

1 The mode of action of lithium on electrical activity in the sympathetic ganglia of the bullfrog has been studied by recording extracellular and intracellular potential changes. Changes in nerve conduction and various types of synaptic transmission were studied when sodium ions in the external solution were totally replaced by equimolar concentrations of lithium ions and also when lithium ions were added to the external Ringer solution.2 Nerve conduction and nicotinic transmission in sympathetic ganglia were completely blocked in sodium-free sucrose solution, but were restored when the preparations were transferred to a sodium-free lithium solution.3 In the sodium-free lithium solution, the slow excitatory postsynaptic potential (e.p.s.p.) and muscarinic acetylcholine-depolarization were restored while the slow inhibitory postsynaptic potential (i.p.s.p.) and the muscarinic acetylcholine-hyperpolarization were not restored. Furthermore, the early after-discharges were accelerated and the inhibition of after-discharges was eliminated. These results support the hypothetical concept that the slow i.p.s.p. is generated by an activation of the electrogenic sodium pump.4 In the sodium-free lithium solution, restoration of nerve conduction and synaptic transmission were transient phenomena; both conduction and transmission were gradually blocked when preparations were soaked in the solution for long periods. The blockade appeared to be due to membrane depolarization.5 When lithium ions (20 mM) were added to the Ringer solution, nicotinic transmission was depressed. The slow e.p.s.p. was also depressed, but less so than the slow i.p.s.p. The early after-discharge was, however, accelerated; presumably due to the marked depression of the slow i.p.s.p. in this solution.6 Changes in synaptic transmission in Ringer solution containing lithium ions could be explained by membrane depolarization, a reduction of acetylcholine release and a depression of the electrogenic sodium pump.7 All results obtained in the present experiments could be explained by supposing that lithium ions are able to substitute for sodium ions in passive ionic membrane transport dependent on electrochemical energy but not in active ionic membrane transport dependent on metabolic energy.

Action Potentials↗