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Biomedical subjects

T Tokimasa

Publications and source records attributed to T Tokimasa.

78 records · Page 5Linked to original sources
PubMed1981

The effect of 5-hydroxytryptamine on the slow inward current of bullfrog atrium.

The effect of 5-hydroxytryptamine (5-HT) on the isometric contraction, membrane potential, and membrane current of isolated bullfrog (Rama catesbeiana) atrium was investigated. 5-HT depressed the isometric contraction and this negative inotropism was atropine-resistant. 5-HT reduced both peak amplitude and duration of the action potential, but caused no detectable changes in the resting membrane potential and membrane input resistance. The final, or "secondary depolarization phase"1) in the rising phase of the action potential was found to be selectively depressed by 5-HT. These inhibitory effects on the action potential was also atropine-resistant. A single sucrose-gap voltage-clamp experiment revealed that 5-HT caused a reduction of the slow inward (Ca++/Na+) current. The membrane slope conductance near the resting membrane potential and the degree of activation of the of the time-dependent potassium current showed no detectable change in the presence of 5-HT. It was concluded on the basis of the present results that 5-HT directly controlled the action potential by selectively depressing the slow inward (Ca++/Na+) current. This may be responsible for the negative inotropic effect of 5-HT on bullfrog atrium.

Acetylcholine↗
PubMed1981

Desensitization of the muscarinic acetylcholine receptor of atrium in bullfrogs.

The membrane of bullfrog atrial muscle is hyperpolarized by an increase of K+ conductance in carbachol-containing Ringer solution. The present experiment demonstrated that both the membrane hyperpolarization and K+ conductance increase showed a decay during prolonged application of carbachol, suggesting desensitization of the muscarinic receptor. Such a decay of the membrane conductance increase was also observed when the membrane potential was clamped at the level of the K+ equilibrium potential; no net flow of K+ across the membrane was expected under such a condition. When carbachol was withdrawn from the external solution after its application for 5-10 min, both the membrane potential and conductance quickly returned to normal control values within 3-4 min, suggesting that the ionic distribution across the membrane also returned to normal. Under such a condition, however, the response to a second application of carbachol was depressed for an extended period. Similarly, decay of the response was observed when carbachol was applied repeatedly for a short period with a short time interval. These results suggested that the muscarinic receptor of the present preparation shows desensitization to carbachol. Similar results were obtained with acetylcholine. The rate of onset of desensitization to carbachol was very slow compared with that of the end-plate; the half-time was 6.62 +/- 2.24 min (mean +/- SD, n=13). This rate, however, was dependent on the membrane potential level and the Ca2+ concentration in the external solution, as in the case of the end-plate, suggesting that the molecular mechanism of desensitization occurring at the receptor-ionic channel complex of the muscarinic receptor of the atrial muscle was comparable with that of the nicotinic receptor of the end-plate.

Acetylcholine↗
PubMed1980

Desensitization of the muscarinic receptor of bullfrog atrial muscle.

The muscarinic ACh receptors, which hyperpolarize the resting membrane and also depress the action potential of bullfrog atrial muscle, show desensitization to the action of ACh. This suggests that the molecular mechanism of these muscarinic ACh receptor-ionic channel (voltage-dependent) complexes is comparable to that of the nicotinic ACh receptor-ionic channel (voltage-independent) complex of the end-plate.

Action Potentials↗