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T Akasu

Publications and source records attributed to T Akasu.

At least 163 records · Page 9Linked to original sources
PubMed1984

Actions of ATP on the soma of bullfrog primary afferent neurons and its modulating action on the GABA-induced response.

Adenosine 5'-triphosphate (ATP) produced a long-lasting depolarization in bullfrog spinal ganglion cells. Since the ATP-induced slow depolarization was associated with an increase in membrane resistance and a reverse in polarity (about--90 mV) which was most likely brought about by an inactivation of membrane potassium conductance. In some cells, a rapid and transient depolarization followed by the long-lasting depolarization was produced by ATP and it was markedly reduced in sodium-free solution. ATP reversibly augmented the GABA-induced depolarization which was caused by ionophoresis of GABA. These observations were confirmed using a voltage clamp method. Dose-response analysis of the action of ATP on the GABA-induced response suggests that the facilitatory action of ATP on the GABA response is effected on the GABA receptor channel complexes without changing the GABA affinity.

Adenosine Triphosphate↗
PubMed1984

Neuropeptides facilitate the desensitization of nicotinic acetylcholine-receptor in frog skeletal muscle endplate.

Substance P and luteinizing hormone-releasing hormone (LHRH), neurotransmitter candidates for peptidergic neurotransmission in peripheral autonomic ganglia, facilitated the desensitization of nicotinic acetylcholine (ACh)-receptor at the skeletal muscle endplate. In the presence of these peptides, the desensitization proceeded with a biphasic time course, i.e. fast and then slow components of desensitization. We suggest that neuropeptides such as substance P and LHRH may regulate the sensitivity of nicotinic ACh-receptors by modulating the process of desensitization.

Acetylcholine↗
PubMed1984

Slow excitatory post-synaptic currents in bull-frog sympathetic neurones.

Electrogenesis of the slow excitatory post-synaptic current (slow e.p.s.c.) was analysed with voltage-clamp methods in curarized sympathetic ganglion cells of bull-frogs. Three types of slow e.p.s.c. were observed from B neurones of sympathetic ganglia. The type I slow e.p.s.c. was associated with a decrease in membrane conductance, was depressed by membrane hyperpolarization and nullified at -60 to -70 mV. It was observed in 65% of the sympathetic neurones studied. The type II slow e.p.s.c. was associated with an increase in membrane conductance, was depressed by membrane depolarization and nullified at around +5 mV. It was observed in 14% of the neurones studied. A third type of slow e.p.s.c. was recorded from 21% of the sympathetic neurones in this study. This slow e.p.s.c. was a mixed type having characteristics of both type I and type II slow e.p.s.c.s. Activation of muscarinic cholinergic receptors by application of acetylcholine (ACh) also produced two types of inward currents. The nature of each type of muscarinic slow ACh current was similar to that of each type of slow e.p.s.c. The time course of the falling phase of type I and type II slow e.p.s.c.s was dependent on the membrane potential. The type I slow e.p.s.c. was primarily dependent on extracellular K+ and appeared to be produced by a suppression of the M-current (Brown & Adams, 1980). The type II slow e.p.s.c. was due to an increased conductance, probably to Na+, and other cations.

Acetylcholine↗
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↗
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

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↗