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Biomedical subjects

T Maeno

Publications and source records attributed to T Maeno.

At least 109 records · Page 6Linked to original sources
PubMed1985

Effects of guanethidine and phenethylguanidine on the frog neuromuscular junction.

The effects of two guanidine derivatives, guanethidine and phenethylguanidine (2-phenyl-ethyl-guanidine), on neuromuscular transmission in the sartorius nerve-muscle preparation of the frog, Rana pipiens, were investigated. Both compounds decreased the peak height of the evoked end-plate current (EPC). The decay of the EPC was changed from a single exponential to a double exponential. The effects of both compounds on the EPC peak height increased with hyperpolarization, and the peak EPC/membrane voltage relationship thus became non-linear. The absence of an effect on the mean quantal content (m) indicated that the two compounds acted postsynaptically. The power spectrum of the ACh-induced noise was changed by guanethidine from a single Lorentzian to a double Lorentzian curve. The single channel conductance was decreased with hyperpolarization. It was concluded from these observations that guanethidine is an open channel blocker. Phenethylguanidine shifted the cut-off frequency of the ACh-induced noise to a higher frequency. However, the power spectrum showed only a single Lorentzian, and there was a lack of low frequency component in the power spectrum, which was expected from the decay phase of the EPC. The single channel conductance decreased, but in contrast to the case of guanethidine, there was no voltage dependency. The possible mechanism of action of phenethylguanidine is discussed.

Acetylcholine↗
PubMed1985

Effects of aniline on neuromuscular transmission.

Aniline hydrochloride increased the amplitude of the end-plate potentials of the frog sartorius muscle. Statistical analysis showed that the effects of aniline were purely presynaptic. The shape of the dose-release curve was similar to that of the 4-aminopyridine curve although the potency was weaker than that of 4-aminopyridine. The molecular configuration and the effect of aniline suggested that the site of action of aniline was the same as that of 4-aminopyridine.

4-Aminopyridine↗
PubMed1985

Excitatory effect of amino acids on identified neuron R14 of Aplysia. I. Glycine-induced depolarization and its ionic mechanism.

The ionic mechanism of the membrane effect of glycine on identified neuron R14 of Aplysia was investigated with conventional intracellular recording and voltage-clamp techniques. Both localized and bath applications of glycine markedly depolarize R14. Bath-applied glycine induced an inward current that gradually reached a maximum and remained at that level until glycine was washed out. Displacement of the holding potential from -46 to -121 mV increased the inward current. The extrapolated reversal potential was +38.6 mV. Reduction of [Na+]o reversibly decreased the inward current. Alterations of [K+]O, [Cl-]O, and [Ca2+]O, as well as bath-applied ouabain and sodium cyanide, did not affect the inward current. These results suggest that glycine can induce an Na+ current and that the glycine-induced inward current does not reflect an active uptake by an Na+-coupled transport system of glycine into the neuron.

Animals↗
PubMed1985

Influences of pressure-injected cyclic AMP on the membrane current and characteristics of an identified neuron of Aplysia kurodai.

The ionic mechanism of the effect of intracellularly injected adenosine 3',5'-cyclic monophosphate (cAMP) on the membrane of identified neuron L5 of Aplysia kurodai was investigated with conventional voltage-clamp and ion-substitution techniques. The intracellular elevation of cAMP caused an inward current (IcAMP), which was not accompanied by a significant change in membrane conductance at potentials more hyperpolarized than -60 mV. The current increased over the voltage range (-50 to -30 mV) associated with a conductance decrease and decreased at potentials more hyperpolarized than -60 mV. Elevated intracellular cAMP was found to enhance a region of negative slope resistance in steady-state I-V relations. Duration of the IcAMP was greatly prolonged by bath-applied isobutylmethylxanthine (50 microM), but imidazole (10 mM) had an opposite effect on the IcAMP. Tolbutamide (5 mM), a protein kinase inhibitor, reduced the IcAMP. The current was not affected by the presence of bath-applied TTX (50 microM), ouabain (50 microM), or triaminopyrimidine (5 mM). Reduction of [Na+]0 reversibly decreased the IcAMP. Li+ could largely substitute for Na+. Alterations of [K+]0, and bath application of 4-AP (5 mM) and TEA (30 mM) did not affect the IcAMP. In the presence of Na+, Cl-, and divalent cations such as Ca2+ and Ba2+ inhibited the IcAMP. These results suggest that fast elevation of intracellular cAMP induces a TTX-resistant slow Na+ inward current, and the current might be due to activation of cAMP-dependent protein kinase.

1-Methyl-3-isobutylxanthine↗
PubMed1984

Ionic mechanism of a hyperpolarizing glutamate effect on two identified neurons in the buccal ganglion of Aplysia.

The ionic mechanism of a membrane effect of L-glutamate on two identified neurons in the buccal ganglion of Aplysia kurodai was investigated with conventional microelectrode techniques and glutamate iontophoresis. Bath-applied and iontophoresed glutamate hyperpolarized the membrane and increased the membrane conductance. The hyperpolarizing glutamate response decreased in amplitude and finally reversed its polarity by conditioning hyperpolarization. The reversal potential of the hyperpolarizing glutamate response was close to the ECl (-60 mV). The reversal potential changed by 22.4 mV when the external chloride concentration was altered by a factor of 5. The relationship between the iontophoretically applied current and the membrane conductance changes was suggestive of two glutamate molecules reacting with a single receptor site. The hyperpolarizing glutamate response was essentially unaffected by 2-amino-4-phosphonobutyric acid (2-APB), L-proline, and quinuclidinyl benzilate (QNB). It was concluded that the hyperpolarizing glutamate response was generated by an activation of Cl- conductance.

Animals↗
PubMed1984

Effects of 5-hydroxytryptamine on membrane potential, contractility, accumulation of cyclic AMP, and Ca2+ movements in anterior aorta and ventricle of Aplysia.

Effects of 5-hydroxytryptamine (serotonin; 5-HT) on the anterior aorta and ventricle muscle of the marine gastropod Aplysia are characterized. Bath-applied 5-HT depolarizes muscle fibers and causes tension increases in both the anterior aorta and ventricle above ca. 10(-9) M. Iontophoretically applied 5-HT caused localized depolarizations of anterior aorta muscle fibers. 5-HT increases the levels of adenosine-3',5'-cyclic monophosphate (cAMP) markedly in the anterior aorta of A. kurodai and A. californica and in the ventricle of A. kurodai. Effects of 5-HT on the contractility of and cAMP synthesis in the anterior aorta and ventricle are both blocked by methysergide. 5-HT and cAMP analogs stimulate 45Ca2+ efflux from the ventricle, implying that the effects of cAMP on contractility involve intracellular Ca2+ movements.

Animals↗
PubMed1983

Catechol and noradrenaline facilitate the neuromuscular transmission via different mechanisms.

Using curarized frog sartorius muscles, selective presynaptic facilitatory effects of two structurally related chemicals, noradrenaline (NA) and catechol (pyrocatechol, PC), were compared by calculating the fractional release (P) from the rundown of endplate potential during a train-of-three stimulation. Below 10 microM, both NA and PC increased P in a similar manner. At higher concentrations, however, the effects of NA were found to be quite different from those of PC. NA never increased further the value of P (0.11-0.13) whereas PC augmented P in a dose dependent fashion up to about 0.76. Thus, the present data suggested that NA and PC facilitate the transmitter release via different mechanisms. The effects of the latter were identical to the case of "chemical potentiation or accelerated evoked release" by 4-aminopyridine.

Animals↗
PubMed1982

Excitatory and inhibitory effects of acetylcholine on the anterior aorta muscle of Aplysia.

The acetylcholine (ACh) responses of anterior aorta muscle cells of Aplysia kurodai were studied by intracellular recording and ACh iontophoresis. Three different types of membrane potential change were observed in response to ACh pulses: a rapid Na+-mediated depolarizing response, a slow, mainly Cl-, in part K+-mediated, hyperpolarizing response, and Na+ (for depolarizing component) and Cl- (for hyperpolarizing component)-mediated biphasic response. The depolarizing response and the depolarizing component of the biphasic response were effectively blocked by hexamethonium or atropine. The hyperpolarizing response and the hyperpolarizing component of the biphasic response were completely blocked by tubocurarine. Low concentrations of ACh inhibited and relaxed the anterior aorta muscle; high concentrations of ACh excited the muscle and initiated contraction. The biphasic responses to ACh are likely due to the presence of more than one ACh receptor type on the same cell membrane of the anterior aorta muscle fiber.

Acetylcholine↗
PubMed1981

Presynaptic effects of 4-aminopyridine and streptomycin on the neuromuscular junction.

Studies were done to assess the effects of 4-aminopyridine (4AP) and streptomycin (SM) on transmitter release parameters and extracellularly recorded presynaptic action potential. The application of 5 micrometer 4AP resulted in a marked increase in the mean quantal content (m1) associated with an increase in the total number of the store of available quanta (n) but had no effect on the probability of release (p) and the fractional release (P). Focal recording showed that 50 micrometer 4AP modified the shape of the presynaptic action potential from a triphasic configuration to a diphasic one. In contrast, prolongation of the muscle action potential was found only at higher concentrations (greater than 1 mM) of of 4AP. Thus, the increase in n with 4 AP was associated with prolongation of the presynaptic action potential evoked by blocking the K current. SM (172 micrometer mM) had no effect on p and P. Reduction of n by SM was completely reversed by 4AP. As the presynaptic action potential change induced by 4AP was not antagonised by SM, it may be that the decrease of n by SM followed a modification of the voltage-dependent Ca channel.

Action Potentials↗
PubMed1981

Kinetic analysis of the action of chemical modulators on neuromuscular transmission.

The kinetics of the direct action of 4-aminopyridine (4AP) and streptomycin (SM) on the mechanism of transmitter release were studied by recording the endplate potentials from curarized frog muscles using conventional microelectrode techniques, and by calculating the fractional release from the store of available acetylcholine quanta from the experiments with tetanic rundown during short train stimulations. To explain the tremendous facilitatory effect of 4AP on the fractional release and the antagonistic interaction of SM thereupon, it was postulated that 4AP and SM modify the transmitter output by combining with the Ca-dependent process X; i.e., 4AP and SM compete for the occupancy of the X site. A combination of 4AP or SM presumably modifies allosterically the action of the Ca-X complex, resulting in a profound augmentation of the evoked release of the available transmitter with the former and its depression with the latter. The theoretically derived equations from the above assumptions agreed reasonably well with the results obtained.

4-Aminopyridine↗
PubMed1980

Ionic mechanism of inhibition of long duration in Aplysia synapse.

In the abdominal ganglion of Aplysia kurodai, three neurons were identified that responded with inhibition of long duration (ILD) to a single stimulation of the siphon nerve and to bath and iontophoretic application of dopamine. The ILD is a long-lasting (15-60 sec) hyperpolarizing potential, typically associated with a conductance increase but with a reversal potential, typically negative than the potassium equilibrium potential. Exchange of half the external chloride with acetate induced no change in the ILD. The ILD was reduced in amplitude in the presence of 0.1 normal K+ in the external medium and enhanced in two times normal K+ solution. The ILD amplitude, but not conductance, was progressively impaired by cooling and by the metabolic inhibitors ouabain and strophanthidin. These results suggest that the ILD is composed of an increase in K++ conductance and activity of the electrogenic Na-pump. theophylline potentiated the ILD, especially its duration. Furthermore, bath application of dibutyryl cAMP augmented the amplitude of the synaptically elicited ILD and the dopamine responses by 30% over controls without any effect on the change in membrane conductance. Intracellularly injected cAMP also increased the ILD, but 5'-AMP showed no such effect. These data suggest that dopamine acts on the ILD neurons by increasing K+ conductance and the activity of the electrogenic Na-pump and that cAMP might selectively stimulate the pump component of the ILD.

Animals↗
PubMed1977

Permeability of the endplate membrane activated by acetylcholine to some organic cations.

The ability of various organic cations to depolarize the ACh-activated endplate membrane in the absence of Na ions was examined on frog sartorius muscle by measuring the endplate potential on the muscle surface with the moving electrode technique. The ACh-activated endplate membrane was very permeable to ammonium and its methyl and hydroxy derivatives, and moderately permeable to guanidine derivatives and Tris (hydroxymethyl) aminomethane. The permeability of alkylol derivatives of ammonium diminished progressively with increase in molecular size. The present results suggested that the endplate ionic channels can be represented by a pore of about 6.4 A in diameter.

Acetylcholine↗