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Biomedical subjects

K Koketsu

Publications and source records attributed to K Koketsu.

At least 55 records · Page 3Linked to original sources
PubMed1981

Antidromic inhibition of acetylcholine release from presynaptic nerve terminals in bullfrog's sympathetic ganglia.

In isolated bullfrog's sympathetic ganglia it was examined if the release of acetylcholine (ACh) from presynaptic nerve terminals was changed when postsynaptic ganglion cells were activated antidromically. The fast excitatory postsynaptic potential (fast EPSP) of ganglion cells was found to be depressed, whereas the nicotinic ACh potential of these cells was not depressed, immediately after these ganglion cells were activated by antidromic axonal or direct intracellular stimulations. This indicates that activation of ganglion cells results in inhibiton of the release of ACh from their presynaptic nerve terminals. Such an antidromic inhibition of ACh release could not be clearly observed when preparations were perfused with Ca2+-deficient solution or when adrenaline (10(-5) M) was added to the superfusion solution. Frequency of the spontaneous miniature EPSP was also found to be decreased after antidromic activation of ganglion cells. On the basis of these results it was concluded that some kind of transmitter was released from activated ganglion cells which inhibited ACh release by acting on preganglionic nerve terminals. This putative neurotransmitter was suggested to be adrenaline.

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↗
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↗
PubMed1980

Oscillation of [Ca2+]i-linked K+ conductance in bullfrog sympathetic ganglion cell is sensitive to intracellular anions.

The intracellular free Ca2+ ([Ca2+]i) regulates the K+ conductance (GK) of the many types of cell membrane. The Ca2+ influx during an action potential activates this [Ca2+]i-linked GK in most neurones. In caffeine-treated sympathetic ganglion cells, however, Ca2+ released from an intracellular Ca2+ reservoir site analogous to the sarcoplasmic reticulum (SR) of the muscle (see ref. 12) causes activation of the GK, which results in slow oscillatory hyperpolarisations (caffeine hyperpolarisation, C-hyperpolarisation). Such a release of Ca2+ linked to the GK of the membrane seems important for understanding the role of the intracellular organelles in the control of membrane activities of a neurone. We report here the mechanism of the slow oscillatory hyperpolarisations recorded from the bullfrog sympathetic ganglion cell in Ringer solution. It is found that these hyperpolarisations are generated by a [Ca2+]i-linked GK system and are highly sensitive to anions in an intracellular recording electrode, probably to intracellular anions.

Animals↗
PubMed1980

Presynaptic regulation of the release of acetylcholine by 5-hydroxytryptamine.

1 The effect of 5-hydroxytryptamine (5-HT) on the release of acetylcholine (ACh) from bullfrog sympathetic preganglionic nerve terminals and frog sciatic nerve terminals was studied with intra-cellular microelectrodes. 2 The change in transmitter release was measured from the mean quantal content calculated by the variance method from evoked fast e.p.s.ps or e.p.ps in low Ca2+-high Mg2+ Ringer solution. 3 5-HT facilitated the release of ACh in low concentrations and depressed it in relatively high concentrations at both preganglionic and motor nerve terminals. 4 These results suggest the possibility that 5-HT may play a role in regulating cholinergic transmission in general.

Acetylcholine↗