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Biomedical subjects

T Akasu

Publications and source records attributed to T Akasu.

At least 181 records · Page 10Linked to original sources
PubMed1982

Modulation of nicotinic transmission by biogenic amines in bullfrog sympathetic ganglia.

Studies of transmission in isolated paravertebral sympathetic ganglia of the bullfrog and at the sciatic-sartarius muscle synapse in the frog yielded evidence that biogenic amines such as catecholamines or 5-hydroxytryptamine can modulate transmission in sympathetic ganglia and at the neuromyal junction. These two transmitter substances are able to modulate transmission by affecting the amount of ACh release from presynaptic terminals and also by affecting the sensitivity of nicotinic Ach receptors of the subsynaptic membrane. Information is presented as to how these compounds exert their modulatory effects on these synapses.

Acetylcholine↗
PubMed1981

Voltage-clamp studies of a slow inward current in bullfrog sympathetic ganglion cells.

Voltage-dependent inward membrane currents of bullfrog sympathetic ganglion cells were analyzed with the voltage clamp method. Two distinct inward currents, a tetrodotoxin (TTX)-sensitive fast inward current (INa) and a TTX-insensitive slow inward current (Isi), were recorded in Ringer solution. The Isi was markedly depressed by removal of external Ca2+ and by the addition of Mn2+, Co2+ or D-600. This suggests that the Isi is, almost exclusively, due to Ca2+. These results indicate that under physiological conditions a Ca2+ influx is induced during initiation of action potentials in these ganglion cells.

Animals↗
PubMed1981

5-hydroxytryptamine controls ACh-receptor sensitivity of bullfrog sympathetic ganglion cells.

Experimental evidences showing that 5-hydroxytryptamine (5-HT) is directly interacting with nicotinic acetylcholine (ACh) receptors and thereby depresses the sensitivity of these receptors to ACh, are presented by making use of bullfrog sympathetic ganglion cells and frog skeletal muscle endplates. It was suggested that 5-HT might decrease the affinity of ACh to nicotinic receptor sites, since the mode of 5-HT action was comparable to that of D-tubocurarine action.

Acetylcholine↗
PubMed1981

Increase of acetylcholine-receptor sensitivity by adenosine triphosphate: a novel action of ATP on ACh-sensitivity.

1. The sensitivity of the nicotinic acetylcholine (ACh)-receptor, measured as the amplitude of ACh-current induced by iontophoretic application of ACh to the frog skeletal muscle endplate, was increased by the action of adenosine triphosphate (ATP). 2. This potentiation was not due to the effect of ATP on ACh-esterase, since the increase of the sensitivity could also be demonstrated by use of carbachol (CCh). 3. Kinetic analysis of the effect of ATP on the dose-response curve of CCh-current suggests that ATP increases the ACh-sensitivity by acting on the allosteric site of receptor-ionic channel complex without changing the affinity of ACh for its recognition site. 4. The equilibrium potential and the life-time of the endplate current (e.p.c.) are not altered by the presence of ATP. 5. These results suggest that ATP increases the ACh-sensitivity by increasing either the conductance of unit channels or the total number of available channels.

Acetylcholine↗
PubMed1978

The effect of adrenaline on the electrogenic Na+ pump in cardiac muscle cells.

Electrogenic Na+ pump currents during K+-activated hyperpolarizations of bullfrog atrium muscle fibres are increased by adrenaline. The log dose-response relation between these currents and activating K+ concentrations is expressed by a sigmoidal curve, which is shifted in parallel to the left by adrenaline. It is suggested that adrenaline increases the rate of Na+ extrusion without increasing the Na/K coupling ratio and total number of pumping sites.

Animals↗
PubMed1977

Effects of dibutyryl cyclic adenosine 3',5'-monophosphate and theophylline on the bullfrog sympathetic ganglion cells.

1 Effects of dibutyryl cyclic adenosine 3',5'-monophosphate (dibutyryl cyclic AMP) and theophylline on bullfrog sympathetic ganglion cells were examined in order to test the hypothesis that cyclic AMP is essential for the generation of slow inhibitory postsynaptic potentials (i.p.s.ps) in these cells. 2 In the absence or presence of theophylline, dibutyryl cyclic AMP did not hyperpolarize but rather tended to depolarize ganglia that were hyperpolarized by adrenaline. 3 Theophylline augmented neither the P-potential (slow i.p.s.p.) nor adrenaline-induced hyperpolarization. 4 Thus, cyclic AMP does not seem to be essential for the generation of the slow i.p.s.p., at least in amphibian sympathetic ganglion cells.

Animals↗
PubMed1977

Activation of electrogenic Na+ pump by epinephrine in bullfrog atrium.

The effects of epinephrine (1 X 10(-6)--1 X 10(-5) M) on the resting membrane potential and the K+-activated hyperpolarization of bullfrog atrial heart muscles were studied by the single sucrose-gap method or by intracellular microelectrode filled with 3 M KC1. Epinephrine-induced hyperpolarization (Ep-hyperpolarization) was completely eliminated by the effect of ouabain or by removal of extracellular K+. The amplitude of K+-activated hyperpolarization, which was produced when the extracellular K+ concentration was raised from zero to 2 mM, was markedly increased in the presence of epinephrine. The membrane depolarizations, due to high extracellular K+ concentration in the presence of ouabain (5 X 10(-6) M) which completely and reversibly eliminated the K+-activated hyperpolarization, were not altered under the effect of epinephrine. These results suggested that Ep-hyperpolarization of bullfrog atrial heart muscles was due to the acceleration of electrogenic Na+ pump which produced the K+-activated hyperpolarization.

Animals↗