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T Maeno

Publications and source records attributed to T Maeno.

At least 91 records · Page 5Linked to original sources
PubMed1989

Intracellularly injected inositol 1,3,4,5,6-pentakisphosphate induces a slow inward current in identified neurons of Aplysia kurodai.

Micropressure injection of inositol 1,3,4,5,6-pentakisphosphate (IP5) into identified neurons (R9-R12) of Aplysia induced a slow inward current associated with a conductance increase. The IP5-induced inward current was decreased by depolarization and increased by hyperpolarization. The extrapolated reversal potential of the current was -11 mV. The IP5-induced inward current was sensitive to changes in [Na+]o, [Ca2+]o and [K+]o but not to changes in [C1-]o, and was resistant to tetrodotoxin. The current was not completely abolished by Ca2+ channel blocking cations, Co2+ and Mn2+. Ion substitution and pharmacological experiments suggest that microinjection of IP5 can activate a non-specific cation conductance in Aplysia neurons.

Animals↗
PubMed1989

Protein kinase C activators reduce the inositol trisphosphate-induced outward current and the Ca2+-activated outward current in identified neurons of Aplysia.

Effects of intracellularly injected activators of protein kinase C on the InsP3-induced K+ current and the Ca2+-activated K+ current recorded from identified neurons (R9-R12) of Aplysia kurodai were investigated with conventional voltage-clamp and pressure-injection techniques. Intracellular injection of InsP3 into identified neurons produced a 4-aminopiridine (4-AP)-resistant, tetraethylammonium (TEA)-sensitive, and quinidine-sensitive K+ current similar to the Ca2+ activated K+ current elicited by direct injection of Ca2+ ions into the same neurons. The diacylglycerol analogue 1,2-oleoylacetylglycerol (OAG) at an intracellular concentration of 65 nM produced irreversible decreases in both the InsP3-induced K+ current and the Ca2+-activated K+ current. The phorbol 12,13-dibutyrate (PDBu) at an intracellular concentration of 150 nM also decreased irreversibly both the InsP3-induced K+ current and the Ca2+-activated K+ current. These results suggest that protein kinase C activators reduce both the InsP3-induced K+ current and the Ca2+-activated K+ current recorded from certain identified neurons of Aplysia and that protein kinase C reduces the ability of Ca2+ to open K+ channels rather than affecting the ability of InsP3 to release Ca2+ from intracellular stores.

4-Aminopyridine↗
PubMed1989

Effect of acetylcholine on ventrocaudal sensory neurons in the pleural ganglia of Aplysia.

1. The effects of acetylcholine (ACh) on the soma of cultured ventrocaudal sensory neurons from the pleural ganglia of Aplysia kurodai were characterized. 2. Whole-cell recording was used for current and voltage clamping. ACh and other drugs were microapplied to the membranes of the cultured neurons. 3. Microapplication of ACh induced an outward current mediated by a conductance increase. No desensitization to repeated applications of ACh was detected. The threshold was 10(-7) M and the maximum response was at 10(-5) M. 4. The reversal potential in normal seawater is -80 mV, close to the K+ equilibrium potential. Increasing [K+]0 shifted the reversal potential by the amount predicted by the Nernst equation. Altering [Cl-]0 did not affect the reversal potential. Thus ACh opens a potassium channel in these sensory neurons and may act as a neurotransmitter on those neurons. 5. Atropine and d-tubocurarine partially blocked the ACh response. Hexamethonium had no obvious effect on this response. Tetraethylammonium reduced the response to 22% of control. Carbamylcholine and arecoline induced outward currents that were 71 and 12%, respectively, of the response to ACh. Nicotine and muscarine had almost no effect. 6. The ACh response was reduced by prior application of serotonin (5HT). The ACh response was also reduced by bath-applied 5HT, forskolin, and isobutylmethylxanthine. These data suggest that ACh activates an "S-like" channel in the ventrocaudal sensory neurons.

Acetylcholine↗
PubMed1989

Comparative bond strengths of plastic teeth to microwave-curing, heat-curing and 4-META containing denture base resins.

Bond strength of hardened plastic teeth or acrylic resin teeth to microwave-curing, conventional heat-curing and 4-META-containing denture base resins were comparatively investigated in this study. Effects of grinding and monomer coating of the tooth ridge lap were also studied. Bond strength of plastic denture teeth to microwave-curing denture base resin was slightly higher than the other two resins. With all denture base resins used, an increased bond strength was obtained with hardened plastic teeth by treatment of tooth ridge lap but not with acrylic resin teeth. However, scattering of the bond strength was reduced by treatment of tooth ridge lap in acrylic resin teeth specimens. With hardened plastic teeth specimens, fracture in the base resin was increased by monomer coating. With acrylic resin teeth specimens, no specific fracture patterns were demonstrated by treatment of tooth ridge lap. Fracture occurred mostly in the acrylic resin teeth. These results suggest that bond strength of both denture teeth to microwave-curing or 4-META-containing denture base resin was increased or solidified by grinding or monomer coating of tooth ridge lap.

Acrylic Resins↗
PubMed1989

Ca-independent augmentation of endplate potential during repetitive stimulation.

To elucidate the role of intracellular Ca ions in neuromuscular transmission, we investigated using frog neuromuscular preparations the effect of 1,2-bis(o-aminophenoxy)ethane- N,N,N',N'-tetraacetic acid (BAPTA) on frequency augmentation-potentiation (formerly frequency facilitation), which have been shown to be useful in identifying the sites of actions of various cholinergic agents. Buffering of intracellular Ca ions by BAPTA was found to suppress only Ca-dependent component of frequency augmentation-potentiation (mo); its stimulation frequency dependent factor (k) remained unaffected. Depression by BAPTA treatment of the short-term facilitation of endplate potential (EPP) was the same in both the resting and augmented states. However, the effect of BAPTA was antagonized, but only partially, with the administration of Ca-ionophore, A23187. These suggest that Ca-buffering capability of the intracellularly loaded BAPTA was maintained during low frequency repetitive stimulation. In addition, the post-tetanic potentiation of miniature EPP frequency in Ca-free EGTA Ringer was practically unaffected with BAPTA treatment. Undoubtedly Ca ions were essential for transmitter release and short-term facilitation, but Ca ions were not solely responsible for all the changes of transmitter release. The contribution of transmitter mobilization to maintaining the synaptic transmission during repetitive stimulation should be reevaluated.

Action Potentials↗
PubMed1988

Kinetic analyses of transmitter release in neuromuscular transmission.

A majority of transmitter quanta in the nerve terminal is in a large pool of store (S), which can be utilized for release only after transformation into activated quanta (n) via two intermediate states called available quanta (A) and releasable quanta (N). Mobilization is a collective term applicable for aggregates of S----A, A----N and N----n conversions. In the present article, various electrophysiological procedures for kinetic analyses of the transmitter release in neuromuscular transmission were discussed to elucidate this not well understood process of mobilization. Especially, frequency augmentation, tetanic rundown and depression, and recovery from depression experiments were proposed to be very useful tools in identifying the drug effect on the mobilization process. Since d-tubocurarine, 2-(4-phenylpiperidino)cyclohexanol (AH5183) and Ba ions satisfied the above three criteria of drug action on mobilization, these were concluded to affect the mobilization of transmitter in neuromuscular transmission.

Animals↗
PubMed1988

Effects of 2-(4-phenylpiperidino)cyclohexanol (AH5183) and barium ions on frog neuromuscular transmission.

1. By applying electrophysiological techniques such as frequency facilitation, tetanic run-down and depression, recovery from depression and post-tetanic potentiation (PTP) of the end-plate potential (EPP), the effects on frog neuromuscular transmission of 2-(4-phenylpiperidino)cyclohexanol (AH5183), a compound known to inhibit specifically the loading of newly synthesized acetylcholine (ACh) molecules into synaptic vesicles, and Ba2+, a selective activator of the augmentation phase of PTP, were investigated to elucidate whether these were related to ACh turnover. 2. Effects of AH5183 and Ba2+ ions were frequency dependent. At low frequency of stimulation, both agents showed essentially no effects on the EPPs recorded from Mg2+-blocked preparations. 3. AH5183 pivoted the log-linear frequency facilitation relation clockwise without altering the intercept on the ordinate, whereas Ba2+ ions did so counter-clockwise. As is the case with Ca2+ ions, Sr2+ ions shifted the relation upwards leaving its slope unaffected. 4. AH5183 selectively depressed the component of potentiation in PTP while the effect of Ba2+ ions was a specific increase in the augmentation phase of PTP. 5. Ba2+ ions increased the amplitude of EPPs in the late depressed phase during the tetanic run-down and depression experiment, but 4-aminopyridine and Ca2+ ions failed to do so. 6. AH5183 increased, Ba2+ ions reduced but Ca2+ ions did not change the constant of recovery from depression of the EPP measured on curarized preparations. 7. The present results suggested that mobilization of the ACh quanta readily available for release might be a common mechanism underlying both frequency facilitation and two components of PTP (augmentation and potentiation). The term 'frequency facilitation' would be more comprehensive if it were re-termed 'frequency augmentation' or 'frequency potentiation'.

4-Aminopyridine↗
PubMed1988

An acetylcholine-induced potassium current in tail sensory neurons in the pleural ganglion of Aplysia.

Acetylcholine (ACh) induces a hyperpolarization during current clamp and an outward current during voltage clamp in tail sensory neurons of Aplysia kurodai. This response was proved to be produced by a specific increase in membrane permeability toward potassium ions, the cholinergic antagonists, d-tubocurarine chloride (d-TC), and atropine mildly reduced the ACh response, while tetraethylammonium (TEA) most effectively blocked this response. These findings provide evidence that tail sensory neurons have the inhibitory ACh receptor in addition to the known receptors for serotonin (5-HT), small cardioactive peptide B (SCPB), and neuropeptide Phe-Met-Arg-Phe-NH2 (FMRFamide).

Acetylcholine↗
PubMed1987

Mechanically induced electrical responses in murine mammary epithelial cells in primary culture.

In mouse mammary epithelial cells in primary culture, mechanical stimulation of a cell induced in other cells within the same colony a short depolarization of less than 15 mV with a duration of 1-8 s and a subsequent, prominent hyperpolarization of 6 mV lasting 10-40 s. Epidermal growth factor induces a spontaneous hyperpolarizing response in cultured mammary cells, and in cells treated with EGF mechanical stimulation produced a greater hyperpolarization, while the amplitude of the depolarizing response was not affected. The amplitude of the mechanically induced hyperpolarization was markedly reduced by quinine and tetraethylammonium, blockers of the Ca2+ -dependent K+ channel. The results suggest that the Ca2+ -dependent K+ channel was involved in the hyperpolarization.

Animals↗
PubMed1987

Effects of synthetic omega-conotoxin, a new type Ca2+ antagonist, on frog and mouse neuromuscular transmission.

A new type Ca2+ antagonist, synthetic omega-conotoxin (omega-CgTX) decreased the peak height of the endplate potential (EPP) in frog muscle but had no effect on the mouse neuromuscular junction. The reduction of endplate potential in frogs was due to a decrease in transmitter release, since the mean quantal content estimated by variance of EPPs (m) and from the peak heights of EPPs and miniature EPPs (m1) was reduced by omega-CgTX, but the postsynaptic sensitivity to ACh was unaltered. The decrease of mean quantal content caused by omega-CgTX was reversed by 4-aminopyridine, guanidine and Bay K 8644. Also, the effect of omega-CgTX was weakened in the presence of 10 mM Ca2+ or 12 mM Mg2+. Statistical analysis revealed that omega-CgTX decreased the number of quanta available (n) whereas the probability of release (p) remained unaffected.

Animals↗
PubMed1987

Forskolin mimics the dopamine-induced K+ conductance increase in identified neurons of Aplysia kurodai.

The ionic mechanism of the effect of micropressure ejection of dopamine (DA) and forskolin on the membranes of identified inhibition of long duration (ILD) neurons of Aplysia kurodai was investigated with conventional voltage-clamp and ion-substitution techniques. Ejection of DA and forskolin onto the neuropil of the ILD neuron produced a slow outward current (5-20 nA in amplitude; 10-60s in duration) associated with a conductance increase. The outward currents induced by DA and forskolin were consistently a linear function of the holding potential, reversing near the predicted potassium equilibrium potential (-80 mV), and were sensitive to changes in the concentration of extracellular K+ but not to extracellular Cl-. Bath-applied isobutylmethylxanthine (50 microM) prolonged the outward current induced by both DA and forskolin, but imidazole (5 mM) had an opposite effect on these currents. Tolbutamide (1-5 mM), a protein kinase inhibitor, reduced the current induced by both DA and forskolin. A antagonist for DA receptors in molluscan neuron, ergometrine maleate, (10 microM) completely abolished the outward current induced by DA, but the current induced by forskolin persisted in the presence of the DA-antagonist. Guanosine 5'O-(2-thiodiphosphate) (GDP beta S, 5-10 microM), an analogue of GDP inhibited the outward current induced by both DA and forskolin. These results suggest that dopamine acts on the ILD neurons of Aplysia kurodai by increasing K+ conductance. Forskolin can mimic the DA action, suggesting that the effect of dopamine is mediated by increased intracellular cAMP.

Action Potentials↗
PubMed1987

Ionic mechanism of the outward current induced by intracellular injection of inositol trisphosphate into Aplysia neurons.

Inositol 1,4,5-trisphosphate (InsP3) has been proposed to be the intracellular second messenger in the mobilization of Ca2+ from intracellular stores in a variety of cell types. The ionic mechanism of the effect of intracellularly injected InsP3 on the membrane of identified neurons (R9-R12) of Aplysia kurodai was investigated with conventional voltage-clamp, pressure-injection, and ion-substitution techniques. Brief pressure injection of InsP3 into a neuron voltage-clamped at -40 mV reproducibly induced an outward current (10-60 sec in duration, 20-60 nA in amplitude) associated with a conductance increase. The current was increased by depolarization and decreased by hyperpolarization up to -80 mV, where it disappeared. Extracellular application of tetraethylammonium (TEA; 5 mM) blocked the InsP3-induced outward current, and the current was not affected by the presence of bath-applied 4-aminopyridine (4-AP; 5 mM). The InsP3-induced outward current recorded at a holding potential of -40 mV increased in amplitude in low-K+ solutions and decreased in amplitude in high-K+ solutions. Alteration of [Cl-]0, as well as perfusion with Ca2+ free plus 2 mM EGTA solution, did not affect the outward current. The InsP3-induced outward current was found to disappear when the neuron was injected with the Ca2+ chelator EGTA. The outward current evoked by repeated InsP3 injection at low doses exhibited summation and facilitation and, at high doses, was shown to desensitize. The calmodulin inhibitor N-(6-amino-hexyl)-5-chloro-1-naphthalene sulfonamide (W-7; 20-50 microM), inhibited both the InsP3-induced and the Ca2+-activated outward currents. An intracellular pressure injection of Ca2+ ions into the same identified neuron was shown to produce an outward current associated with a K+ conductance increase similar to the InsP3-induced current, and the current was blocked by bath-applied TEA (5mM). These results suggest that brief pressure injection of InsP3 into certain identified neurons of Aplysia induces a 4-AP-resistant, TEA-sensitive K+ current activated by increased intracellular free Ca2+ concentration, and this increase might be the result of the mobilization of Ca2+ from intracellular stores by InsP3.

4-Aminopyridine↗
PubMed1987

[Uneven fractionation irradiation].

To get the better therapeutic ratio with low LET radiation therapy alone, the improvement of the physical dose distribution and the mode of dose fractionation are required. Since 1972, uneven fractionation irradiation with electron beam has been used for head and neck tumors. The 2 year control rates for primary tongue cancer T1, T2 and T3 by this method were approximately comparable to that of the small source implantation. In the treatment results for the cervical lymph node metastasis, uneven fractionation technique is superior to conventional one. Furthermore, this results was reviewed by means of multivariate analysis.

Analysis of Variance↗
PubMed1986

Effects of memantine on the frog neuromuscular junction.

The effects of memantine, an adamantane derivative, on neuromuscular transmission in the frog sartorius muscle preparation were studied by measuring the endplate current (EPC) by the voltage clamp method. Memantine (0.5-50 microM) reduced the peak amplitude and shortened the duration of the EPC, and the membrane voltage-peak EPC relationship became non-linear. Since it decreased the quantal height of the EPC without affecting the mean quantal content, the effects were considered to be mainly postsynaptic. Noise analysis revealed that memantine decreased the mean lifetime of the ACh-activated channel. In addition, lineweaver-Burk analysis of the response to ionophoretically applied carbamylcholine showed that memantine acted essentially as a linear mixed-type inhibitor. Thus memantine seems to block neuromuscular transmission by reacting with the ACh receptor-ion channel complex in both the open and closed states.

Acetylcholine↗
PubMed1986

Involvement of the Ca2+-dependent K+ channel activity in the hyperpolarizing response induced by epidermal growth factor in mammary epithelial cells.

Epidermal growth factor (EGF) induces a hyperpolarizing response of 5-20 mV amplitude in mouse mammary epithelial cells in culture. The amplitude of the hyperpolarizing response was reduced by more than 60% within several minutes after addition of blockers of voltage and/or Ca2+-dependent K+ channels such as tetraethylammonium (7 mM) or quinine (0.29 mM). Both nifedipine (0.15 mM), a blocker of the Ca2+ channel, and ruthenium red (2 mM), an inhibitor of the Ca2+-binding site, also reduced the amplitude of the hyperpolarizing response by more than 60%. The Ca2+ ionophore, A23187 (3.8 microM), induced a large hyperpolarization, which was 25-40 mV and lasted about 3 min. These data suggest that activity of the Ca2+-dependent K+ channel was involved in the EGF-induced hyperpolarizing response of the mammary epithelial cells.

Animals↗
PubMed1986

Catechol: a potent and specific inhibitor of the fast potassium channel in frog primary afferent neurones.

The effects of catechol on various ionic channels of isolated primary afferent neurones of the bull-frog were examined by a single-suction-electrode clamp system, which combined internal perfusion and current or voltage clamp using an electronic switching circuit. Catechol was found to inhibit rather specifically the fast K+ current as does 4-aminopyridine (4-AP). Ca2+, Na+ and slow K+ currents were not affected. Although both 4-AP and catechol were inhibitors of the fast K+ channels, their sites of action were quite different. Catechol was effective when applied on the external surface of the cell membrane whereas 4-AP acted preferably internally. We assumed that a single fast K+ channel has two distinct sites for blockers: the catechol site is exposed to the external medium or situated at the outer orifice of the pore, and the 4-AP site is located within the same channel but is more easily accessible from inside the nerve cell than outside. The 4-AP and catechol sites were not, however, completely separate and independent of each other since a synergistic interaction was observed between catechol and 4-AP.

4-Aminopyridine↗