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E Kumamoto

Publications and source records attributed to E Kumamoto.

16 recordsLinked to original sources
PubMed1991

Short-term facilitation as a tool to know neuromodulator-induced change in Ca2+ movement in the nerve terminal.

A theory was developed to show how we can predict the actions of neuromodulators on Ca2+ movement (yo: impulse-induced increase in Ca2+ concentration; c: basal Ca2+ level) in the nerve terminal from their effects on an impulse-evoked transmitter release (m: quantal content) and short-term facilitation (F) elicited by paired impulses, based on the simplest version of the residual Ca2+ hypothesis of facilitation. It was demonstrated from this theory that yo should be increased (decreased) when both m and F were increased (decreased) and that c should be increased (decreased) when m and F were increased (decreased) and decreased (increased), respectively. These ideas could interpret some published experimental results well.

Animals↗
PubMed1991

Long-term potentiation induced by a sustained rise in the intraterminal Ca2+ in bull-frog sympathetic ganglia.

1. The mechanism of a long-term potentiation of transmitter release (pre-LTP) induced by a tetanic stimulation (33 Hz for 1-30 s) applied to the preganglionic nerve was examined by intracellularly recording the fast excitatory postsynaptic potentials (fast EPSPs) in bull-frog sympathetic ganglia. 2. Short-term facilitation induced by paired pulses was decreased during the course of pre-LTP; the extent of reduction paralleled with the magnitude of pre-LTP. 3. The frequency of miniature EPSPs increased after tetanic stimulation that produced the pre-LTP. 4. The Ca2+ ionophore, A23187, increased both the amplitude and quantal content of fast EPSPs and frequency of miniature EPSPs while it decreased short-term facilitation. 5. A Ca2+ chelating agent, Quin-2, loaded as acetoxymethyl ester, reduced the amplitude and quantal content of fast EPSPs and short-term facilitation, and blocked the generation of pre-LTP. 6. Activators of protein kinase C, phorbol 12,13-dibutyrate and 1-oleoyl-2-acetyl-rac-glycerol, and its inhibitors, H-7 and staurosporine, did not block the generation of pre-LTP, while the activators enhanced transmitter release. 7. Inhibitors of calmodulin, trifluoperazine and W-7, blocked the generation of pre-LTP, whereas the amplitude and quantal content of fast EPSPs were not influenced. 8. These results suggest that the pre-LTP results from a sustained rise in the basal level of intraterminal Ca2+ and an activation of the Ca(2+)-calmodulin-dependent process in the preganglionic nerve terminals.

Animals↗
PubMed1990

Slow inward and late slow outward currents induced by hyperpolarizing pre-pulses in cat bladder parasympathetic neurones.

Single-electrode voltage-clamp techniques were used to examine membrane currents recorded as a result of hyperpolarizing pre-pulses in cat bladder parasympathetic neurones. In 84 ganglion cells examined, two types of current were observed in response to hyperpolarizing pre-pulses of 10 ms to 1 s duration from holding potentials of -30 to -60 mV to test potentials of -90 to -130 mV. In 46 cells, a short-duration pulse induced a slow inward current (SIC); with longer pulse durations, an outward current was superimposed on the SIC, resulting in a late slow outward current (LSOC). In the remaining cells, either a SIC (n = 12) or an LSOC (n = 26) was recorded over a range of hyperpolarizing pre-pulse durations. The more depolarized the holding potential, the more hyperpolarized the test potential and the longer the pulse duration, the larger the amplitude of the SIC and LSOC. The SIC and LSOC were associated with an increase in input conductance. The extrapolated reversal potential (Vrev) for the LSOC obtained at a holding potential of -60 mV (where the LSOC seemed to be less contaminated with the SIC) was -89 +/- 4 mV (mean +/- standard error of the mean; n = 5), which is close to the equilibrium potential for the K ion. The LSOC was depressed by a high-K (10-20 mM) solution and potentiated by a low-K (0.47 mM) solution. The SIC was depressed by a low-Na (26.2 mM) solution, but was not affected significantly by a low-Cl (12.2 mM) solution. A low-Ca (0.1 mM)/high-Mg (5 mM) solution depressed the LSOC, while a high-Ca (5 mM) solution potentiated it. Cd (0.5 mM) blocked the SIC almost completely, and suppressed the LSOC. The LSOC but not the SIC was suppressed by tetraethylammonium chloride (10 mM). Superfusing Cs (3 mM) did not affect either the LSOC or the SIC. 4-Aminopyridine (1 mM) and muscarine (10 microM) depressed or replaced the SIC with an outward current, while potentiating the LSOC. These results suggest that a hyperpolarizing pre-pulse induces slow inward Na- and late slow outward Ca-dependent K currents, which are inactivated at depolarized potentials and are de-inactivated by hyperpolarizing pulses in a time-dependent manner.

4-Aminopyridine↗
PubMed1990

Action of an irreversible acetylcholine esterase inhibitor, soman, on muscarinic hyperpolarization in cat bladder parasympathetic ganglia.

1. Intracellular recording techniques were used to examine the action of an irreversible acetylcholine esterase (AChE) inhibitor, soman, on the hyperpolarizations mediated through muscarinic cholinoceptors in cat bladder parasympathetic neurones. 2. Soman (0.1-10 microM) depressed the amplitude and prolonged the duration of the muscarinic slow inhibitory postsynaptic potential (s-i.p.s.p.) elicited by a preganglionic tetanus (40 Hz for 1 s) in the presence of mecamylamine (20 microM), phentolamine (1 microM) and caffeine (1 mM), in a dose-dependent manner. The effect of soman on the amplitude of the s-i.p.s.p. was partially reversible, while the effect on the duration was irreversible. 3. Soman hyperpolarized the membrane and decreased input resistance, but this effect could not account for soman-induced inhibition of the s-i.p.s.p. 4. Soman depressed the amplitude and prolonged the duration of a muscarinic hyperpolarization induced by pressure application of acetylcholine (ACh) in the presence of mecamylamine, phentolamine and caffeine. The time course of this effect paralleled that on the synaptically-evoked muscarinic s-i.p.s.p. 5. A reversible AChE inhibitor, pyridostigmine (10-100 microM), also depressed the amplitude and prolonged the duration of a muscarinic hyperpolarization induced by either preganglionic stimulation or ACh pressure application. These actions were reversible, and not accompanied by a significant change in membrane potential or input resistance. 6. The inhibitory action of soman (1 microM) on the muscarinic hyperpolarization was prevented by pyridostigmine (10 microM), but not by atropine (1 microM). 7. These results demonstrate that soman prolongs not only the muscarinic hyperpolarization, but also inhibits its amplitude through a postsynaptic action, probably through AChE inhibition, in cat bladder parasympathetic neurones.

Acetylcholine↗
PubMed1989

Patch clamp experiments on nicotinic acetylcholine receptor-ion channels in bullfrog sympathetic ganglion cells.

Nicotinic acetylcholine-receptor ion channels (AChR channels) were studied in bullfrog sympathetic ganglion cells cultured for 1 day to 3 weeks, using a patch clamp technique. Microsuperfusion of ACh (2-10 microM) to the ganglion cell under the whole cell clamp produced an inward current at membrane potentials negative to -60 mV, which had a fast onset and decay. This rapid ACh-induced current was accompanied by a large current fluctuation, decreased and increased in amplitude by membrane depolarization and hyperpolarization, respectively, and blocked by d-tubocurarine. Thus, this current must be induced by the nicotinic action of ACh, but not by a muscarinic effect to activate a slow cation-selective current. At depolarized levels more than -50 mV, ACh induced an additional inward current which was slow in time course, accompanied by no or decreased current fluctuation and increased in amplitude by membrane depolarization. Accordingly, this slow ACh-induced current could result from the suppression of a voltage-dependent K+ current (M-current: Brown and Adams 1980) by the muscarinic action of ACh. Fluctuation analysis of the rapid ACh-induced current at potentials negative to -50 mV revealed the elementary conductance of 14 pS and a power spectral density distribution of the double Lorentzian function which yielded the time constants of 5.4 and 62.5 ms at -60 to -80 mV. The variance of either component was independent of the mean current.

Acetylcholine↗
PubMed1989

Synaptic potentials induced by postganglionic stimulations in cat bladder parasympathetic neurones.

Intracellular recording techniques were used to examine and compare synaptic potentials evoked by stimulating pre- and postganglionic nerve trunks in cat bladder parasympathetic ganglia. In the 76 ganglion cells examined, two types of responses were recorded on stimulating the postganglionic nerve: an antidromic action potential (type PostNS1; n = 30) or a fast excitatory postsynaptic potential (f-EPSP; type PostNS2; n = 46) which resulted in an orthodromic-like action potential. In some of the cells exhibiting a PostNS1 response (n = 19), a fast depolarization was superimposed on the antidromic spike. This depolarization was due to the synaptic activation of nicotinic receptors. In many of the cells exhibiting either PostNS1 or PostNS2 responses, repetitive stimulation of the postganglionic nerve induced a slow hyperpolarization. Applying nicotinic (hexamethonium, 0.5-1 mM) receptor muscarinic (atropine, 1 microM), alpha-adrenergic (phentolamine, 1 microM) and purinergic (caffeine, 0.5-1 mM) receptor antagonists completely inhibited the tetanus-induced slow hyperpolarization in some cells (n = 5). In other cells (n = 15), a slow hyperpolarization persisted in the presence of these antagonists. These results indicate that stimulation of the postganglionic nerve trunk of cat bladder parasympathetic ganglia can elicit not only an antidromic action potential, but also synaptic potentials which are mediated by the activation of cholinergic (nicotinic and muscarinic), noradrenergic and purinergic receptors, as well as non-cholinergic, non-alpha-adrenergic and non-purinergic synaptic potential.

Animals↗
PubMed1989

Synaptic structure and axon collaterals of type B neurons in bullfrog sympathetic ganglia: intracellular horseradish peroxidase (HRP)-labeling study.

Type B neurons of the bullfrog sympathetic ganglia were examined to confirm the existence of axon collaterals and the distribution of synaptic contacts using the intracellular horseradish peroxidase (HRP) labeling method. The mean diameter of the perikarya was 60.8 (+/- 11.5 standard deviation; n = 36) X 43.8 (+/- 11.3) microns and the mean diameter of the initial segments of axons was 6.0 (+/- 1.8; n = 36) microns. Axon collaterals were found in 6 cells among 36 examined. They branched from axons at 61-167 microns from the perikaryon of origin. Short-axon collaterals containing vesicles (diameter: about 70 nm) were also observed to protrude from the stem axons. Spine-like processes were observed from the cell soma, axon hillock and the initial segment of the axon. They enclosed synaptic axon varicosities, or extended into the extracellular space without any synaptic contact. Serial sections revealed 171 axon varicosities in contact with a single ganglion cell; 32 (18.7%) varicosities were seen on the somata. 66 (38.6%) on the axon hillock and 73 (42.7%) on the initial segment of the axon which extended 100 microns from the perikaryon. Synaptic terminals were also found on the axon as far as 494 microns from the cell body of origin. These findings would provide a morphological basis for interaction between bullfrog sympathetic neurons at pre- or postsynaptic sites.

Animals↗
PubMed1989

Fast hyperpolarization following an excitatory postsynaptic potential in cat bladder parasympathetic neurons.

Intracellular recording techniques were used to study a fast hyperpolarizing potential following the fast excitatory postsynaptic potential evoked by an orthodromic nerve stimulation in cat bladder parasympathetic ganglion cells. In the 61 ganglion cells examined, two types of responses were recorded on stimulating the preganglionic nerve; one had only a fast excitatory postsynaptic potential (type SI, n = 20) and the other had a fast excitatory postsynaptic potential followed by a fast hyperpolarizing potential (type SII, n = 41). In type SII neurons, the half-maximum duration of the afterhyperpolarizing potential following an orthodromic spike was longer than that of a direct spike produced by injecting a depolarizing current pulse through the recording electrode; the half-maximum durations for afterhyperpolarizing potentials following orthodromic and direct action potentials were comparable in type SI cells. Blocking the initiation of an orthodromic spike by hyperpolarizing the membrane in type SII cells revealed a fast excitatory postsynaptic potential followed by a fast hyperpolarizing potential which was similar to that observed at the resting potential. The fast hyperpolarizing potential had a duration comparable to that of an afterhyperpolarizing potential following an orthodromic action potential. The fast excitatory postsynaptic potential-fast hyperpolarizing potential sequence was blocked completely and reversibly by nicotinic receptor antagonists (hexamethonium and D-tubocurarine). Atropine, alpha-2 noradrenergic (yohimbine and phentolamine), and purinergic (caffeine) antagonists had no effect on the fast hyperpolarizing potential. In cells which show type SII responses, spontaneous excitatory postsynaptic potentials were not followed by a hyperpolarization. Depolarizing the membrane (by passing a cathodal current through the recording electrode) to an amplitude comparable to that of a fast excitatory postsynaptic potential also did not elicit a membrane hyperpolarization in type SII cells. In some cells, stimulating one preganglionic nerve trunk elicited a fast hyperpolarizing potential, but activating another nerve trunk innervating the same ganglion cell did not. There was no correlation between the variations in the amplitudes of the fast excitatory postsynaptic potential and the fast hyperpolarizing potential in type SII cells, but increasing the stimulus intensity applied to the presynaptic nerve fiber potentiated the amplitude of the fast excitatory postsynaptic potential and the fast hyperpolarizing potential. The fast hyperpolarizing potential was not associated with appreciable changes in input resistance.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1986

Mechanism of long-term potentiation of transmitter release induced by adrenaline in bullfrog sympathetic ganglia.

A mechanism of the long-term potentiation of transmitter release induced by adrenaline (ALTP) was studied by recording intracellularly the fast excitatory postsynaptic potentials (fast EPSPs). The ALTP was produced during the blockade of K+ channels at the presynaptic terminals by tetraethylammonium (TEA). The synaptic delay, possibly reflecting a relative change in the duration of an action potential at the presynaptic terminal, was not changed during the course of the ALTP. By contrast, it was significantly lengthened by TEA and other K+ channel inhibitors (4-aminopyridine and Cs+) that markedly enhanced the evoked release of transmitter. The magnitude of facilitation of the fast EPSP, induced by a conditional stimulus to the preganglionic nerve, was decreased during the generation of the ALTP, but was unchanged during the potentiation of transmitter release caused by TEA. These results, together with theoretical considerations applying the residual Ca2+ hypothesis to the facilitation, suggest that the enhancement of transmitter release during the ALTP is not caused by an increased Ca2+ influx during a presynaptic impulse owing to the blockade of K+ channel or the modulation of Ca2+ channel, but presumably is induced by a rise in the basal level of free Ca2+ in the presynaptic terminal.

Animals↗
PubMed1986

Long-term potentiation of transmitter release induced by adrenaline in bull-frog sympathetic ganglia.

Long-term potentiation (l.t.p.) of transmitter release induced by adrenaline in bull-frog sympathetic ganglia was studied using intracellular recording techniques. The quantal content of the fast excitatory post-synaptic potentials (fast e.p.s.p.s: evoked by the nicotinic action of acetylcholine) was potentiated for more than several hours after treatment with adrenaline (1-100 microM). A similar l.t.p. of quantal content was produced consistently by isoprenaline (10 microM) and only in a certain fraction of cells by dopamine (10 microM). The l.t.p. induced by adrenaline (10 microM) was blocked by a beta-antagonist, propranolol (1 microM), but not by an alpha-antagonist, phenoxybenzamine (1 microM). Dibutyryl adenosine 3',5'-phosphate (dibutyryl cyclic AMP) (0.8-1.0 mM), adenosine 3',5'-phosphate (cyclic AMP) (4 mM), 3-isobutyl-1-methylxanthine (10 microM), caffeine (1-2 mM), and cholera toxin (2 micrograms ml-1) applied for 20-30 min, all caused the l.t.p. of quantal content. By contrast, adenosine 5'-phosphate (AMP) (4 mM) and adenosine (4 mM) had no potentiating action. Treatment of the ganglion with adrenaline (2.5-160 microM) or dibutyryl cyclic AMP (4 mM) for 15-30 min resulted in the l.t.p. of the frequency of miniature e.p.s.p.s. The l.t.p. of quantal content induced by adrenaline was markedly suppressed by lowering temperature from 20-25 degrees C to 11-13 degrees C, and blocked by dibutyryl guanosine 3',5'-phosphate (dibutyryl cyclic GMP) (100 microM) consistently when applied together, but inconsistently when given after adrenaline. The post-synaptic sensitivity to acetylcholine was unchanged for at least 1 h after exposure to adrenaline (2.5-160 microM) or dibutyryl cyclic AMP (0.8-4 mM). It can be concluded that adrenaline produces l.t.p. of transmitter release by activating a cyclic-AMP-dependent metabolic process through the activation of beta-adrenoceptors, and that this mechanism is presumably regulated by a process involving endogenous guanosine 3',5'-phosphate (cyclic GMP).

1-Methyl-3-isobutylxanthine↗
PubMed1985

The mechanism of the inhibitory action of adrenaline on transmitter release in bullfrog sympathetic ganglia: independence of cyclic AMP and calcium ions.

The effects of adrenaline and dibutyryl adenosine 3':5' - cyclic monophosphate (db cyclic AMP) on nicotinic transmission in bullfrog sympathetic ganglia were compared by use of an intracellular recording technique. The evoked release of transmitter, acetylcholine (ACh), was decreased in the presence of adrenaline (10-100 microM), while the postsynaptic sensitivity to ACh was unchanged (10 microM adrenaline) or slightly reduced (100 microM). Transmitter release was similarly inhibited by dopamine (10 microM), but not by isoprenaline (10 microM). The inhibitory action of adrenaline on transmitter release was blocked by phenoxybenzamine but not by propranolol. The inhibition of transmitter release was independent of the external calcium concentration. The evoked release of transmitter and the electrical properties of the postsynaptic membrane were unchanged during exposure to db cyclic AMP (1-4 mM), while the postsynaptic sensitivity to ACh was slightly but significantly depressed. The spontaneous release of transmitter in a high K+ (10 mM) solution was decreased in the presence of adrenaline (100-300 microM), but unchanged with db cyclic AMP (4 mM). In contrast to the effects during exposure, both the evoked and spontaneous release of transmitter were enhanced after the removal of adrenaline or db cyclic AMP. Neither adrenaline (100 microM) nor db cyclic AMP (4 mM) affected the presynaptic spike and synaptic delay. It is concluded that adrenaline mainly inhibits the release of ACh from the presynaptic terminals through its alpha-action, while db cyclic AMP reduces slightly the postsynaptic sensitivity to ACh and that both agents facilitate transmitter release when they are removed from the presynaptic terminals. It is further suggested that the inhibitory action of adrenaline is independent of endogenous cyclic AMP and calcium ions.

Acetylcholine↗
PubMed1985

Effects of K+-channel blockers on transmitter release in bullfrog sympathetic ganglia.

Effects of K+-channel blockers, tetraethylammonium (TEA), 4-aminopyridine (4-AP) and Cs+ on synaptic transmission were studied with an intracellular electrode in bullfrog sympathetic ganglia. TEA (25-500 microM), 4-AP (0.6-5 microM) and Cs+ (50 microM-10 mM) all increased the quantal content of the fast excitatory postsynaptic potential in a dose-dependent manner. The effects of TEA were rapid in onset and recovery, whereas those of 4-AP and Cs+ appeared with a notable delay and reversed slowly. All blockers lengthened synaptic delay. When compared at approximately equipotent concentrations for potentiation of transmitter release, TEA and 4-AP were found to produce a similar lengthening of the synaptic delay whereas Cs+ caused a much greater prolongation. The quantal size of the fast excitatory postsynaptic potential and the amplitude of the acetylcholine potential were not affected by 4-AP or Cs+, but were depressed by TEA. These results indicate that TEA, 4-AP and Cs+ enhance evoked transmitter release in bullfrog sympathetic ganglia. It is suggested that the potentiation is caused, at least in part, by a mechanism that increases Ca++ influx in the nerve terminal. The enhanced influx is presumed to be mediated by a broadening of the presynaptic action potential after K+-channel blockade.

4-Aminopyridine↗