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K Koketsu

Publications and source records attributed to K Koketsu.

At least 37 records · Page 2Linked to original sources
PubMed1983

Modulation of action potential during the late slow excitatory postsynaptic potential in bullfrog sympathetic ganglia.

The spike peak and after-hyperpolarization of the action potential of bullfrog sympathetic ganglion cells were depressed during the late slow excitatory postsynaptic potential (EPSP). These changes in the action potential were mimicked by luteinizing hormone-releasing hormone (LH-RH), a neurotransmitter candidate for the late slow EPSP. LH-RH (5 microM) suppressed the voltage-dependent K+ currents, both the delayed rectifier K+ current (IK1) and the M current (IK2). It is suggested that the depression of the after-hyperpolarization of the action potential during the late slow EPSP may be due to suppression of IK1 and IK2.

Action Potentials↗
PubMed1983

Luteinizing hormone-releasing hormone modulates nicotinic ACh-receptor sensitivity in amphibian cholinergic transmission.

Luteinizing hormone-releasing hormone (LH-RH; 100 nM-50 microM) reduced the sensitivity of the nicotinic ACh-receptor in amphibian sympathetic ganglion cells and skeletal muscle end-plates. Analyses of LH-RH action, based on a Michaelis-Menten type kinetics, revealed that LH-RH depressed the maximum response (Vmax) of the dose-response curve of ACh currents without changing the affinity (Km) of ACh to the receptor. It was suggested that LH-RH reduced the sensitivity of nicotinic receptor by acting on a certain allosteric site of the receptor-ionic channel complex. Probably, LH-RH reduces the ACh current by decreasing the number of channels available.

Animals↗
PubMed1983

Substance P inhibits the action potentials in bullfrog sympathetic ganglion cells.

Substance P (0.5-5 microM) depressed the spike peak and after-hyperpolarization of action potentials of bullfrog sympathetic ganglion cells. It also depressed the after-hyperpolarization and prolonged the falling phase in Ca2+ spikes. The voltage-dependent K+ currents, both the delayed rectifier K+ current (Ik1) and the M current (Ik2), were suppressed by substance P, suggesting that the depression of the after-hyperpolarization may be due to suppression of these K+ currents.

Action Potentials↗
PubMed1983

Effects of serotonin (5-hydroxytryptamine) on amphibian neuromuscular junction.

A study of the effects of serotonin transmission was carried out on the frog neuromuscular junction by means of microelectrode methods. Serotonin was employed in concentrations of 5-100 microM. Serotonin did not affect membrane characteristics or the resting potential whether at non-neuronal (muscular fiber) or endplate segments of the junction. While serotonin did not affect the frequency of the miniature endplate potentials (MEPPs), it significantly decreased evoked release of acetylcholine. Serotonin significantly decreased, in a dose-dependent fashion, the amplitude of acetylcholine potentials, endplate currents (EPCs), endplate potentials (EPPs) and MEPPs. Also, serotonin shortened significantly the EPC time course and half-decay time, and caused loss of membrane voltage sensitivity of the half-decay time. While it did not affect the null potential, serotonin changed the voltage-EPC relationship from linear to non-linear, and markedly attenuated the dependence of EPC amplitude on membrane potential. These results demonstrate that serotonin induces depressant effects at both pre- and post-synaptic sites of amphibian neuromuscular junction and that its post-synaptic action is directed at the receptor-channel macromolecule rather than at either the channel or the receptor alone.

Acetylcholine↗
PubMed1983

Modulatory actions of ATP on membrane potentials of bullfrog sympathetic ganglion cells.

Adenosine triphosphate (ATP) depolarized the membrane of bullfrog sympathetic ganglion cells by decreasing resting K+ conductance. ATP also depressed the maximum amplitude of after-hyperpolarization of action potentials. Voltage-clamp study revealed that ATP markedly suppressed the TEA-insensitive K+ current which appeared to correspond to the M-current, while it affected less significantly on the delayed rectifier K+ current. It was suggested that ATP depolarized resting membrane by suppressing resting K+ conductances, including the M-current, and also depressed the after-hyperpolarization of action potentials by suppressing both the M-current and delayed rectifier K+ current.

Action Potentials↗
PubMed1983

Substance P modulates the sensitivity of the nicotinic receptor in amphibian cholinergic transmission.

The effect of substance P on the sensitivity of nicotinic acetylcholine (ACh) receptors of bullfrog sympathetic ganglion cells and frog skeletal muscle endplate was examined electrophysiologically. The amplitude of ACh-induced postsynaptic potential (ACh potential) and current (ACh current) were reversibly and dose-dependently reduced by substance P at low concentrations (0.42-42 microM). The mean amplitude of the miniature endplate potential (m.e.p.p.) was also reduced by substance P (4.2 microM). Substance P (4.2 microM) shifted the S-shaped dose-response curve of the ACh current downward. A Lineweaver-Burk plot constructed from the dose-response curve revealed that substance P depressed the maximum response (Vmax) without changing the apparent affinity (Km) of ACh for the receptor. Substance P (0.42-42 microM) did not alter the reversal potential of the ACh current of the endplate. The half-decay time of endplate current (e.p.c.) and its voltage-dependency were not altered by substance P in these concentrations. The depression of the ACh current by substance P may not be due to a blockade of the opened channel which has been activated by the preceding combination of ACh with the receptor. These results suggest that substance P suppresses the sensitivity of nicotinic ACh-receptors of the sympathetic ganglion cell and skeletal muscle endplate, acting on a certain allosteric site but not the recognition site of ACh in the receptor-ionic channel complex.

Animals↗
PubMed1983

Electrogenesis of the slow inhibitory postsynaptic potential in bullfrog sympathetic ganglia.

The ionic mechanisms of the slow surface positive (P)-potential and the slow inhibitory postsynaptic potential (IPSP), an intracellularly recorded P-potential in sympathetic ganglia, were analysed by means of sucrose-gap, intracellular microelectrode techniques, and voltage clamp technique. Both the P-potential and the slow IPSP consist of two different potential components, namely the ouabain-sensitive and the ouabain-insensitive components. The ouabain-sensitive component was enhanced by a moderate conditioning hyperpolarization. This component was most reasonably explained as a potential change generated by an activation of the electrogenic Na+ pump. The ouabain-insensitive potential component of the P-potential and the slow IPSP decreased in the amplitude and finally reversed its polarity by conditioning hyperpolarization. The reversal potential of ouabain-insensitive component of slow IPSP and slow inhibitory postsynaptic current (IPSC) was close to the EK. The amplitude of ouabain-insensitive component of P-potential and slow IPSP was markedly decreased by an elevation of external K+ concentration. The reversal potential of ouabain-insensitive component shifted to a more positive potential level in high K+ Ringer's solution. On the other hand, it was augmented in K+-free Ringer's solution. A reduction of the membrane resistance was observed during the generation of the slow IPSP, when the membrane potential of ganglion cells was held at a membrane potential level more negative than -60 mV. The slow IPSC recorded by voltage-clamp method was associated with an increase in membrane conductance. It was concluded that the ouabain-insensitive component was generated by an activation of K+ conductance.

Animals↗
PubMed1983

Prolonged action potential of frog skeletal muscle membrane in Ca-free EGTA solution.

The membrane of isolated frog skeletal muscle fibers with or without T-system is depolarized to about -30 mV in a Ca-free solution containing 2 mM EGTA. Under such a condition, the action potential can be produced by a cathodal pulse when the membrane is previously hyperpolarized to -70- -100 mV by a conditioning anodal current. The action potential consists of two different potential components, namely a spike potential and a following slow depolarizing response forming a plateau phase (plateau potential). The membrane conductance during the plateau potential is increased. Both spike and plateau potentials are abolished in the absence of NaCl. TTX blocks a spike potential without affecting a plateau potential, whereas Mn and D-600 act contrarily. The i-v relation shows an anomalous rectification in Na-free solution, suggesting that the K conductance during the plateau phase is decreased. It is suggested that spike and plateau potentials are produced by a movement of sodium ions through sodium and calcium channels of the membrane, respectively.

Action Potentials↗
PubMed1982

Biogenic antagonists of the nicotinic receptor: their interactions with erabutoxin.

The hypothesis that the sensitivity of the nicotinic ACh-receptor is reduced by some neurotransmitters was evaluated by studying the interaction between these neurotransmitters and erabutoxin-b (ETX-b), known to bind irreversibly with the specific ACh-receptor site. It was found that the blocking action of ETX-b was apparently prevented by previous application of 5-HT, whereas it was not prevented by application of catecholamine (CA). These results indicate that 5-HT blocks the nicotinic ACh-receptor by interacting with the specific ACh binding site, whereas CA blocks it by interacting with an allosteric site of the ACh-receptor ionic channel complex.

Acetylcholine↗
PubMed1982

Effects of histamine on acetylcholine release in bullfrog sympathetic ganglia.

The effects of histamine on the release of acetylcholine (ACh) from bullfrog sympathetic preganglionic nerve terminals were examined by means of intracellular microelectrode techniques. Low concentrations of histamine (1, 3 muM) increased the amplitude of fast excitatory postsynaptic potentials (fast EPSPs) and ACh quantal content, while high concentrations (100, 300 muM) decreased the amplitude and content. Amplitudes of miniature EPSPs and ACh potentials were not affected by histamine (0.3-300 muM). The facilitatory effect of histamine on fast EPSPs disappeared in the presence of mepyramine, whereas the depressant effect of histamine on fast EPSPs disappeared in the presence of cimetidine. These results suggest that histamine has facilitatory and depressant actions on ACh release. The facilitatory action is probably mediated by the H1-receptor and the depressant action by the H2-receptor, both of which are located at the presynaptic nerve terminals of bullfrog sympathetic ganglia.

Acetylcholine↗
PubMed1982

Identification of gK systems activated by [Ca2+].

Rhythmic caffeine hyperpolarizations generated in bullfrog sympathetic ganglion cells are assumed to be caused by periodic increase in gK due to rise in [Ca2+]i7--9,13. Caffeine-induced outward currents seem to be composed of two different components, which show different pharmacological natures and also different dependencies on membrane potential changes. These two components may be generated by activation of two voltage-dependent K+ currents, namely IK1 (the delayed rectifier K+ current) and IK2 (IM) of ganglion cells. These results suggested that at least two different gK systems were activated by [Ca2+]i in sympathetic ganglion cells.

Acetylcholine↗
PubMed1982

Modulation of voltage-dependent currents by muscarinic receptor in sympathetic neurones of bullfrog.

The muscarinic actions of acetylcholine (ACh) on the action potentials of bullfrog sympathetic ganglion cells were studied with voltage-clamp experiments. The slow inward current (Isi) carried by Ca2+ was markedly depressed by ACh. ACh also markedly depressed the time-dependent outward current following Isi. The outward current was composed of two components, a TEA-sensitive rectifier K+ current (IK1) and a TEA-insensitive slow rectifier K+ current (IK2). Both of these components were depressed by ACh.

Acetylcholine↗
PubMed1982

A kinetic analysis of the facilitatory action of adrenaline.

The 22Na+-efflux from skeletal muscle cells of frog (Rana nigromaculata) was measured in Ringer solutions containing different concentrations of K+ (0.1 to 30 mM). The effects of adrenaline (30 microM) and ouabain (10 microM) on the 22Na+-efflux were investigated for the purpose to clarify the mechanism of the facilitatory effect of adrenaline on Na+ - K+ pump. The rate coefficient for the ouabain-sensitive 22 Na+-efflux increases with increasing extracellular K+ concentrations and adrenaline potently facilitates these rate coefficients. On the basis of Michaelis-Menten type kinetics assumed for the reaction between pump site and extracellular K+, it is concluded that adrenaline decreases the dissociation constant (Km), and increases the maximum Na+-efflux.

Animals↗
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↗
PubMed1982

Presynaptic muscarinic receptors inhibiting active acetylcholine release in the bullfrog sympathetic ganglion.

1 The effects of bethanechol and atropine on the release of acetylcholine (ACh) from bullfrog sympathetic preganglionic nerve terminals were examined electrophysiologically. 2 Bethanechol (1 mM) caused no depolarization of sympathetic preganglionic nerve terminals, whereas carbachol or ACh in the same concentration induced marked depolarizations of these terminals. 3 Bethanechol (10 microM) depressed the amplitude of fast excitatory postsynaptic potentials (e.p.s.ps) recorded in Ca2+-high Mg2+ solution, without depolarizing ganglion cells. The quantal content measured from these fast e.p.s.ps by the variance method showed a significant reduction. 4 Amplitudes of both miniature e.p.s.ps and ACh-potentials induced by iontophoresis of ACh were not affected by addition of bethanechol (10 microM). 5 The depressant effect of bethanechol (10 microM) on fast e.ps.ps disappeared in the presence of atropine (3 microM). 6 Atropine (3 microM) increased the quantal content measured from fast e.p.s.ps recorded in low Ca2+-high Mg2+ solution. 7 The depressant effect of bethanechol (10 microM) on fast e.p.s.ps was unaffected by alpha-adrenoceptor blocking agents (phenoxybenzamine (10 microM) or phentolamine (10 microM). 8 These results suggest that presynaptic nerve terminals in bullfrog sympathetic ganglia possess a muscarinic receptor which inhibits active release of ACh.

Acetylcholine↗
PubMed1982

Desensitization of the muscarinic receptor controlling action potential of bullfrog atrial muscles.

Action potentials of the bullfrog atrial muscle, being depressed by carbachol in concentrations of (1-5) X 10(-7) M, were found to show a slow recovery when application of the drug was sustained. The rate of onset of recovery largely varied depending on individual preparations. The recovery of action potentials was neither due to changes in the ionic distribution across the membrane nor to a secondary action of catecholamine which was released by the nicotinic action of carbachol on sympathetic nerve terminals. These results suggested that the muscarinic ACh receptor responsible for the depression of action potentials showed desensitization to the action of its agonist. The slow inward current recorded by the voltage-clamp experiment showed a decrease and subsequent slow recovery in the presence of carbachol. This suggested that the muscarinic ACh receptor associating with the ionic channel of the slow inward current showed desensitization. It may be suggested on the basis of these experimental results that 1) the muscarinic ACh receptor of bullfrog atrial muscle may compose a receptor-ionic channel complex (RICC) with voltage-dependent CA2+ channel and 2) the molecular reaction between this RICC and agonist may be comparable to that occurring in the nicotinic RICC of the frog end-plate.

Acetylcholine↗