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T Maeno

Publications and source records attributed to T Maeno.

At least 73 records · Page 4Linked to original sources
PubMed1992

Activation of K+ current in macrophages by platelet activating factor.

Puff application of platelet activating factor (10(-8) M) onto peritoneal macrophages from thioglycollate-stimulated mice induced an outward current at a holding potential of -63 mV. The current was suppressed by an antagonist Y-24180 but not by CV-3988. Charybdotoxin (10(-6) M) suppressed the current. Reversal potentials were dependent on external K+ concentrations. The current was not suppressed in Ca(2+)-free EGTA-containing solution but was completely abolished in BAPTA-AM containing solution. These results suggest that platelet activating factor activates a Ca(2+)-dependent K+ channel.

Animals↗
PubMed1992

Effects of hyperthermia on intracellular calcium concentration and responses of cancerous mammary cells in culture.

Effects of hyperthermia on the intracellular calcium concentration (Cai) of an established mouse breast cancer cell line, MMT060562, were studied using fura-2 fluorescence microscopy and the whole-cell clamp technique. A sudden change of temperature from 37 to 45 degrees C induced a transient increase in the fluorescence ratio permeability of the cell membrane and inward current. Deletion of extracellular calcium abolished the fluorescence ratio response to the rise in temperature. Cai of some cells increased after hyperthermia treatment at 44-48 degrees C for 20 min, but the average increase of Cai was negligible. After hyperthermia treatment, spontaneous oscillation of Cai, chemical responses to ATP and bradykinin and the mechanically-induced spreading response diminished. However, the mechanically induced increase of Cai within the stimulated cell remained even after hyperthermia treatment. Suppression of the ATP-induced Cai response recovered to about half the original level within 12 h. Blockage of protein synthesis with cycloheximide (100 microM) had no effect on the recovery. The D-myo-inositol 1,4,5-triphosphate (IP3)-dependent increase of Cai remained intact even after hyperthermia treatment. It is concluded that hyperthermia treatment increases both the permeability of the cell membrane and Cai, but decreases the sensitivity of cells to ATP and bradykinin, presumably due to modification of the signal transduction mechanism.

Adenosine Triphosphate↗
PubMed1992

Reduction of the acetylcholine-induced K+ current in identified Aplysia neurons by human interleukin-1 and interleukin-2.

1. Effects of bath-applied recombinant human interleukin-1 (rhIL-1) and interleukin-2 (rhIL-2) on the acetylcholine (ACh)-induced K+ current recorded from identified neurons (R9 and R10) of Aplysia kurodai were investigated with voltage-clamp and pressure ejection techniques. 2. Bath-applied rhIL-1 and rhIL-2 (10-40 U/ml) reduced the ACh-induced current in the neurons without affecting the resting membrane conductance and holding current. 3. The suppressing effects of these cytokines on the current were completely reversible. 4. Heat-inactivated rhIL-1 and rhIL-2 were without effect. 5. These results suggest that the immunomodulators, IL-1 and IL-2, can modulate the ACh-induced response in the nervous system.

Acetylcholine↗
PubMed1992

Mechanically induced electrical and intracellular calcium responses in normal and cancerous mammary cells.

Mechanically induced channel activities and increase of intracellular calcium ([Ca2+]i) in normal and cancerous murine mammary cells (MMT 060562) were investigated using the patch clamp technique and Fura-2 fluorescence. Both cell types showed similar properties. Upon mechanical stimulation, activation of the Ca(2+)-dependent K+ channel or outward membrane current was recorded in cells which were several cells distant from the stimulated cell. Mechanical stimulation also induced an increase of [Ca2+]i in the touched cell, and this increase of [Ca2+]i spread to the surrounding cells. The [Ca2+]i signal travelled a distance of 100-200 microns within 20-40 s and then diminished. The presence of cell-to-cell communication between adjacent mammary cells through gap junction was indicated by injection of lucifer yellow and measurements of electrical coupling (coupling constant = 0.2-0.3). The mechanically induced increase of the [Ca2+]i signal spread to adjacent cells even when the stimulated cell had no physical contact with them. In the absence of fluid movement, the pattern of the spread of the [Ca2+]i signal was a concentric circle. However, in the presence of fluid movement, the pattern changed to elongate to the direction of the flow. These findings suggested that a certain factor was released from the mechanically stimulated cell to the extracellular space, and this factor induces the increase of [Ca2+]i in surrounding cells.

Animals↗
PubMed1992

Effects of toki-shakuyaku-san (Tsumura TJ-23) on electrical activity in neuroblastoma cells and frog neuromuscular junctions.

Toki-shakuyaku-san (Tsumura TJ-23) is a Chinese medicine which has been used for the treatment of gynecological symptoms in aged women. There are several reports on the usefulness of this drug in the treatment of cognitive disorders. We studied the effects of toki-shakuyaku-san on electrical activity in NG108-15 cells, a cell line of differentiated neuroblastoma x glioma hybrid cells, and on frog neuromuscular transmission. In the hybrid cells, an extract of toki-shakuyaku-san slightly depolarized the membrane potential, and strongly decreased the peak heights of the Na+ and Ca2+ current components of the action potential. The order of potency for NG108-15 cells of the 5 ingredients in toki-shakuyaku-san was soujyutsu >> shakuyaku, takusha, toki, senkyu. In voltage-clamped NG108-15 cells, toki-shakuyaku-san and soujyutsu decreased the Na+, K+, and Ca2+ current components. Toki-shakuyaku-san and soujyutsu also induced an increase in the intracellular calcium concentration. However, toki-shakuyaku-san did not affect neuromuscular transmission in the frog sartorius muscle. The results suggest that the effects of toki-shakuyaku-san on neurons are multiple, and tissue- and species-specific, and its effect derives mainly from soujyutsu.

Action Potentials↗
PubMed1992

[Cardiac performance in total anomalous pulmonary venous connection].

Cardiac performance in 54 patients with total anomalous pulmonary venous connection was investigated by cardiac catheterization before and after surgery. 51 patients underwent intracardiac repair, and 17 of them died during or immediately after operation. According to the preoperative study, the left ventricular ejection fraction (LVEF) of surviving patients was significantly higher than that of patients who died, and the pulmonary arterial mean pressure of surviving patients was significantly lower than that of patients who died. However, there was no significant difference between the left ventricular end-diastolic volume (LVEDV), right ventricular ejection fraction (RVEF), and right ventricular end-diastolic volume (RVEDV) in surviving patients and those who died. Post-operative catheterization studies showed significant increases of LVEF and LVEDV compared to pre-operative figures. RVEF and RVEDV and pulmonary arterial mean pressure decreased significantly after surgery. It was concluded that preoperative cardiac performance of surviving patients was better than that of those who died, and post-operative cardiac performance of surviving patients was basically normal.

Blood Pressure↗
PubMed1991

Tumor necrosis factor reduces the ACh-induced outward current in identified Aplysia neurons.

Effects of extracellularly applied recombinant human tumor necrosis factor (rhTNF) on the acetylcholine (ACh)-induced K+ current recorded from identified neurons (R9 and R10) of Aplysia kurodai were investigated with conventional voltage-clamp and pressure ejection techniques. Bath-applied rhTNF (200-500 U/ml) reduced the ACh-induced current in the neurons without affecting the holding current and resting membrane conductance. The suppressing effect of rhTNF on the current was completely reversible. Inhibition by rhTNF was non-competitive. Heat-inactivated rhTNF was without effect. Our results suggest that the immunomodulator TNF can act on the ACh receptor in the nervous system.

Acetylcholine↗
PubMed1991

Ionic mechanism of the outward current induced by extracellular ejection of interleukin-1 onto identified neurons of Aplysia.

The ionic mechanism of the effect of extracellularly ejected recombinant human interleukin-1-beta (rhIL-1) on the membrane of identified neurons R9 and R10 of Aplysia was investigated with voltage-clamp, micropressure-ejection, and ion substitution techniques. Micropressure-ejected rhIL-1 caused a marked hyperpolarization in the unclamped neuron. Clamping the same neuron at its resting potential level (-60 mV) and reejecting rhIL-1 with the same dose produced a slow outward current (I0(IL-1), 20-30 s in duration, 3-5 nA in amplitude) associated with a decrease in input membrane conductance. I0(IL-1) was decreased by depolarization and increased by hyperpolarization. The extrapolated reversal potential of I0(IL-1) was approximately +15 mV. I0(IL-1) was sensitive to changes in the external Na+ concentration but not to changes in K+, Ca2+ and Cl- concentrations, and was resistant to tetraethylammonium (5 mM) and 4-aminopyridine (5 mM). Neither perfusion of the neuron with 50 microM tetrodotoxin nor perfusion with 10 mM Co2+ seawater caused any changes in I0(IL-1). I0(IL-1) was partially reduced by 50 microM ouabain. These results suggest that extracellular IL-1 can induce a slow outward current associated with a decrease in Na+ conductance and the immunomodulator IL-1 can act directly on the nervous system as well as on the immune system.

Animals↗
PubMed1991

Analysis of a decreased Na+ conductance by tumor necrosis factor in identified neurons of Aplysia kurodai.

The ionic mechanisms of the effect of extracellularly ejected recombinant human tumor necrosis factor-alpha (rhTNF-alpha) on the membrane of identified neurons R9 and R10 of Aplysia kurodai was investigated with conventional voltage-clamp, micropressure ejection, and ion substitution techniques. Micropressure-ejected rhTNF caused a marked hyperpolarization in the unclamped neuron. Clamping the same neuron at it resting potential level (-60 mV) and reejecting rhTNF-alpha with the same dose produced a slow outward current [Io (TNF)] associated with a decrease in input membrane conductance. Io (TNF) was decreased by depolarization and increased by hyperpolarization. The extrapolated reversal potential of Io (TNF) was approximately +10 mV. Ion substitution and pharmacological experiments suggest that Io (TNF) in identified neurons R9 and R10 of A. kurodai is due to a decreased Na+ conductance but not due to an activation of the Na(+)-K+ pump. Our results demonstrate that the immunomodulator TNF can act directly on the nervous system as well as on the immune system.

Animals↗
PubMed1991

The activation of Ca(2+)-dependent K+ conductance by adrenaline in mouse peritoneal macrophages.

Responses to adrenaline in mouse peritoneal macrophages were investigated with perforated and cell-attached patch-clamp recording, and with a combination of the perforated-patch recording and fura-2 fluorescence measurements. Extracellularly applied adrenaline induced a transient outward current (4-10 s in duration, 100-500 pA in amplitude) at -40 mV associated with a marked increase in conductance. The adrenaline-induced current [Io (Adr)] reversed polarity near -80 mV. The reversal potential depended distinctly on the external K+ concentration but not on external Cl- concentration. Removal of external Ca2+ did not affect Io(Adr) within 2-4 min but subsequent responses to adrenaline were progressively depressed. In contrast, treatment with an intracellular Ca2+ chelator, the acetoxymethyl ester of 1,2-bis-(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid completely abolished Io(Adr). Furthermore, Io(Adr) was blocked by bath-applied quinidine and charybdotoxin, but not by tetraethylammonium or apamin. Extracellular application of an alpha 1-adrenoceptor agonist phenylephrine and of noradrenaline mimicked Io(Adr). On the other hand, Io(Adr) was antagonized by a non-selective alpha-adrenoceptor antagonist phentolamine (0.2 microM) and an alpha 1-adrenoceptor antagonist prazosin (0.2 microM), but was not affected by an alpha 2-adrenoceptor antagonist yohimbine (1 microM) or a beta-adrenoceptor antagonist propranolol (1 microM). Cell-attached single-channel recordings with the pipette solution containing 145 mM KCl revealed the activation of single-channel currents with a conductance of 40 pS during application of adrenaline outside the patch. Parallel measurements of membrane current and fura-2 fluorescence in the same cell demonstrated a correlation between the rise in [Ca2+]i and an increase in K+ conductance. Therefore, it is concluded that adrenaline activates a Ca(2+)-dependent K+ conductance by release of Ca2+ from internal stores through an activation of an alpha 1-adrenoceptor.

Animals↗
PubMed1991

Oscillating activity of a calcium-activated K+ channel in normal and cancerous mammary cells in culture.

Calcium-activated potassium channels were the channels most frequently observed in primary cultured normal mammary cell and in the established mammary tumor cell, MMT060562. In both cells, single-channel and whole-cell clamp recordings sometimes showed slow oscillations of the Ca2(+)-gated K+ current. The characteristics of the Ca2(+)-activated K+ channels in normal and cancerous mammary cells were quite similar. The slope conductances changed from 8 to 70 pS depending on the mode of recording and the ionic composition in the patch electrode. The open probability of this channel increased between 0.1 to 1 microM of the intracellular Ca2+, but it was independent of the membrane potential. Charybdotoxin reduced the activity of the Ca2(+)-activated K+ channel and the oscillation of the membrane current, but apamin had no apparent effect. The application of tetraethylammonium (TEA) from outside and BaCl2 from inside of the cell diminished the activity of the channel. The properties of this channel were different from those of both the large conductance (BK or MAXI K) and small conductance (SK) type Ca2(+)-activated K+ channels.

Animals↗
PubMed1991

[Tissue plasminogen activator treatment of postvitrectomy pupillary fibrin membrane].

Twenty-five micrograms of human recombinant tissue plasminogen activator (tPA) was injected via the corneoscleral limbus of 14 postvitrectomy aphakic eyes with prominent pupillary fibrin membranes. Fibrinolysis by tPA was initiated by thirty minutes after the injection, and the fibrin membrane was completely dissolved within sixty minutes. No toxicity attributed to tPA was observed clinically. Intraocular fluid was obtained during fluid-gas exchange after complete dissolution of fibrin and analyzed for decomposed fibrin products (FDP). Intraocular FDP was significantly higher (160 +/- 250 micrograms/ml) than normal after tPA treatment. Intraocular tPA administration is a potent modality to treat postvitrectomy fibrin membrane. Fluid-gas exchange must be performed to eliminate as much FDP as possible to reduce postoperative inflammation.

Adolescent↗
PubMed1990

Extracellular tumor necrosis factor induces a decreased K+ conductance in an identified neuron of Aplysia kurodai.

Recombinant human tumor necrosis factor (rhTNF) was pressure-applied onto the the soma of identified neuron R12 in the Aplysia abdominal ganglion. rhTNF induced a slow inward current (ITNF, 80-100 s in duration, 5-10 nA in amplitude) associated with a conductance decrease. ITNF begins 1-2 s after applying rhTNF and peaks in 5-6 s. ITNF was decreased by hyperpolarization and had a reversal potential of approximately -87 mV (close to the K+ equilibrium potential). Ion substitution and pharmacological experiments suggest that ITNF is due to a decreased K+ conductance and that TNF, a product of macrophages, may form an important link in communications between nervous and immune systems.

Animals↗
PubMed1990

Activation of single Ca2(+)-dependent K+ channel by external ATP in mouse macrophages.

Single Ca2(+)-dependent K+ currents responding to external ATP were recorded from cell-attached patches on mouse peritoneal macrophages. Extracellularly applied ATP activated an inward single-channel current with a conductance of 25 pS and a reversal potential of -79 mV (pipette potential, Vp) when the pipette contained a 145 mM KCl solution. The reversal potential was shifted 56 mV positive by a 10-fold reduction in external (pipette) K+ concentration. The effect of ATP was abolished by either removal of external Ca2+ or treatment with an intracellular Ca2+ chelator, the acetoxymethyl ester of 1,2-bis (2-aminophenoxy)ethane-N,N,N'N'-tetraacetic acid (BAPTA-AM). This channel has a mean open time of 9.1 ms and open probability was not strongly dependent on Vp in the range tested (+120 to -30 mV).

Adenosine Triphosphate↗
PubMed1990

Activation of a non-specific cation conductance by intracellular injection of inositol 1,3,4,5-tetrakisphosphate into identified neurons of Aplysia.

The ionic mechanism of the effect of intracellularly injected inositol 1,3,4,5-tetrakisphosphate (IP4) on the membrane of identified neurons (R9-R12) of Aplysia kurodai was investigated with conventional voltage-clamp, pressure injection, and ion-substitution techniques. Intracellular injection of IP4 into a neuron voltage-clamped at -45 mV reproducibly induced a slow inward current (20-60 s in duration, 3-5 nA in amplitude) associated with a conductance increase. The current was decreased by depolarization and increased by hyperpolarization. The extrapolated reversal potential was -21 mV. The IP4-induced inward current was sensitive to changes in the external Na+, Ca2+ and K+ concentration but not to changes in Cl- concentration, and was resistant to tetrodotoxin (50 microM). When the cell was perfused with tetraethylammonium (5 mM) but not with 4-aminopyridine (5 mM), the IP4-induced inward current recorded at -45 mV slightly increased. The IP4-induced inward current was partially reduced by calcium channel blockers (Co2+ and Mn2+). These results suggest that intracellularly injected IP4 can activate a non-specific cation conductance.

Animals↗
PubMed1990

Extracellular ATP activates Ca2(+)-dependent K+ conductance via Ca2+ influx in mouse macrophages.

1. Using the perforated patch recording, the effects of ATP on membrane current were investigated in mouse peritoneal macrophages. 2. Extracellularly applied ATP induced a biphasic current consisting of a initial inward current [Ii(ATP)] followed by an outward current [Io(ATP)]. These currents were associated with a marked increase in conductance at their peaks. 3. Ii(ATP) reversed close to 0 mV and was attenuated by removal of external Na+. 4. Io(ATP) reversed near -80 mV and was increased by decreasing the external concentration of K+. 5. Io(ATP) was completely abolished by removal of external Ca2+, treatment with an intracellular Ca2+ chelator, the acetoxymethyl ester of 1,2-bis (2-aminophenoxy) ethane-N,N,N',N'-tetra acetic acid (BAPTA-AM) and bath applied quinidine but not tetraethylammonium (TEA) or apamin. 6. These results suggest that Ii(ATP) and Io(ATP) are due to an activation of nonspecific cationic and Ca2(+)-dependent K+ conductances, respectively, and raise the possibility that the putative ATP receptor may be important in regulating macrophage functions, motility, phagocytosis and cytokines secretion.

Adenosine Triphosphate↗
PubMed1989

Intracellularly injected inositol hexakisphosphate induces a biphasic current in identified neurons of Aplysia.

Inositol hexakisphosphate (IP6) was pressure-injected into the somata of the identified neurons (R9-R12) in the abdominal ganglion of Aplysia. Intracellular injection of IP6 into a neuron voltage-clamped at -45 mV reproducibly induced a biphasic membrane current consisting of an inward current (Ii(IP6)) followed by a slow outward current (Io(IP6)). Conductance is increased at the peaks of these currents. The extrapolated reversal potential of Ii(IP6) was -34 mV, whereas Io(IP6) was increased by depolarization and decreased by hyperpolarization up to -75 mV, where it disappeared. Ion substitution and pharmacological experiments suggest that microinjection of IP6 into the Aplysia neurons activates two or more separate types of ion channels.

Animals↗