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Biomedical subjects

N Motohashi

Publications and source records attributed to N Motohashi.

At least 55 records · Page 3Linked to original sources
PubMed1996

Decreased inositol 1,4,5-trisphosphate-specific binding in platelets from alcoholic subjects.

We measured the degree of inositol 1,4,5-triphosphate (IP3)-specific binding in platelets from alcoholic and nonalcoholic subjects. IP3-specific binding in alcoholic subjects was 45% less than that in nonalcoholic subjects. There was no significant difference in the number of IP3 receptors as detected immunologically in the platelet membrane fractions from alcoholic and nonalcoholic subjects. These results indicate that the decrease in IP3-specific binding in alcoholic subjects may have been due to a decreased affinity, but not number of IP3 binding sites. In contrast to the decrease in IP3 receptor binding, there were no significant changes in phospholipase-C activity or immunoreactivity of phospholipase C-beta 1 in platelet membranes from alcoholic subjects. The decreased IP3-specific binding in platelets may allow for the development of biological markers for alcoholism.

Adult↗
PubMed1996

gamma-Aminobutyric acid increases intracellular Ca2+ concentration in cultured cortical neurons: role of Cl- transport.

The effect of gamma-aminobutyric acid (GABA) on intracellular Ca2+ concentration ([Ca2+]i) in cultured prenatal rat cortical neurons was investigated using fluorescence imaging. GABA or muscimol, but not baclofen, increased [Ca2+]i in a dose-dependent manner. The GABAA receptor antagonists, bicuculline and picrotoxin, inhibited the GABA response. Furosemide, an inhibitor of the Na+/K+/2Cl- cotransporter, inhibited the GABA response in a noncompetitive manner. Ethacrynic acid, an inhibitor of an ATP-dependent Cl- pump, also inhibited the GABA-induced increased in [Ca2+]i. These results suggest a role for Cl- transport processes in the GABA response. The coapplication of GABA and high K+ led to a non-additive increase in the GABA response. The GABA response was also inhibited by nifedipine, a voltage-gated Ca2+ channel blocker, and abolished by the absence of extracellular Ca2+. Results indicate that the GABA response shares a common pathway of Ca2+ movement with the high K(+)-induced response. These observations suggest that the stimulation with GABA results in Ca2+ influx through voltage-gated Ca2+ channels, and that these effects are dependent on Cl- transport systems.

Animals↗
PubMed1996

Three-dimensional dental cast analyzing system using laser scanning.

The purpose of this article is to introduce the outline of our newly developed three-dimensional dental cast analyzing system with laser scanning, and its preliminary clinical applications. The system is composed of a measuring device with a slit-ray laser projector and two sets of coupled charged devised video cameras, an image processing unit, a 16-bit personal computer as a controller, and an engineering workstation as a post processor. The dental cast is projected and scanned with a slit-ray laser beam. The raster coordinates of the target are determined with an image processor. Triangulation is applied to determine the location of each point. Generation of three-dimensional graphics of the dental cast takes approximately 40 minutes. About 90,000 sets of X, Y, Z coordinates are stored in the main memory of the microcomputer. The measurement error is less than 0.05 mm. Besides the conventional linear and angular measurements of the dental cast, we are also able to demonstrate the size of the palatal surface area and the volume of the oral cavity. The advantage of this system is that it facilitates the otherwise complicated and time-consuming mock surgery necessary for treatment planning in orthognathic surgery.

Computer Graphics↗
PubMed1996

Effects of clomipramine and verapamil on 5-HT-induced intracellular calcium changes in individual C6 rat glioma cells.

The effects of antidepressants and calcium (Ca2+) antagonists on serotonin (5-HT)-induced Ca2+ increase were investigated in single C6BU-1 glioma cells with digital imaging microscopy. Application of 5-HT (100 nM-100 microM) caused a rapid and reversible rise of intracellular Ca2+ concentration ([Ca2+]i) in a concentration-dependent manner. In the absence of extracellular Ca2+, the sustained phase of the [Ca2+]i response was strongly reduced, which was greater than the suppression of the initial peak. This suggests that the peak value is mainly due to internal Ca2+ storage sites, and the sustained phase is mainly composed of Ca2+ influx. The sustained phase was significantly attenuated by 100 nM clomipramine and verapamil. The present findings demonstrate that clomipramine and verapamil, in their therapeutic concentrations, have a common action of inhibiting Ca2+ influx, and suggest that the calcium antagonistic effect may play an important role in clinical effects of antidepressants.

Animals↗
PubMed1996

Effects of chronic ethanol treatment on inositol 1,4,5-trisphosphate receptors and inositol 1,3,4,5-tetrakisphosphate receptors in rat brain.

In this study, the effects of chronic ethanol treatment on inositol 1,4,5-trisphosphate (IP3) and inositol 1,3,4,5-tetrakisphosphate (IP4) specific binding in rat brain was investigated. In the cerebellum, chronic, but not acute, ethanol treatment caused a decrease in the number IP3 receptors. The effect of chronic ethanol treatment on IP3 and IP3 receptor mRNA levels was also studied in order to determine the mechanisms responsible for the decrease in IP3 receptor binding. Chronic ethanol treatment did not change IP3 levels, indicating that the decrease of IP3 receptors is not caused by the alteration of IP3 levels. Also IP3 receptor mRNA levels had no change after chronic ethanol treatment. These findings suggest that the decrease in IP3 receptors in the cerebellum could be caused by either a decrease in the translation of IP3 receptor mRNA or an increase in proteolysis of IP3 receptors. In contrast, chronic ethanol treatment had no effect on the Bmax or Kd of IP4 specific binding in the cerebellum. It is speculated that a change at the level of the IP3 receptor in the cerebellum may be associated with the development of adaptation and tolerance to chronic ethanol exposure.

Animals↗
PubMed1995

Inhibition of serotonin-induced Ca2+ mobilization by interleukin-1 beta in rat C6BU-1 glioma cells.

To study the potential interaction between cytokine and serotonin (5-HT) signal transduction, we evaluated the effect of interleukin-1 beta (IL-1 beta) on the 5-HT2 receptor-mediated mobilization of intracellular Ca2+ in cultured rat C6BU-1 glioma cells. Pretreatment of cells with IL-1 beta significantly inhibited the 5-HT-induced mobilization of Ca2+ in a dose (30-1000 U/ml)- and time (12-24 h)-dependent manner. Inhibition was observed when cells were stimulated with concentrations of 5-HT of > or = 1 microM, which induced the maximal 5-HT response. Lipopolysaccharide (1 microgram/ml) also inhibited 5-HT-induced Ca2+ mobilization, but heat-inactivated IL-1 beta as well as interferon-alpha (1000 U/ml), interferon-gamma (1000 U/ml), and tumor necrosis factor-alpha (2000 U/ml) did not. The inhibitory effects of IL-1 beta and LPS were significantly prevented by genistein, a selective tyrosine kinase antagonist, and by H7, a potent inhibitor of protein kinase C. These results indicate that IL-1 beta and LPS inhibit 5-HT2 receptor-mediated Ca2+ mobilization via pathways that include the activation of a tyrosine kinase and protein kinase C. The interaction between cytokines (IL-1 beta) and monoamines (5-HT) may serve to modulate signal transduction in the central nervous system.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1995

Cyclic GMP generation mediated by 5-HT-2 receptors via nitric oxide-dependent pathway and its effect on the desensitization of 5-HT-2 receptors in C6 glioma cells.

Serotonin (5-HT)-2 receptor-mediated cGMP generation was investigated in comparison with calcium (Ca2+) mobilization in C6 glioma cells. 5-HT enhanced cGMP generation, and risperidone and ketanserin potently blocked the response. These results indicate that 5-HT-2 receptors are responsible for the cGMP generation. 5-HT-induced cGMP production was completely abolished by BAPTA, an intracellular Ca2+ chelating agent, or NG-mono-methyl-L-arginine(NMMA), a nitric oxide synthase (NOS) inhibitor, suggesting that 5-HT-induced cGMP generation was through nitric oxide (NO)-dependent pathway. 5-HT (10 microM)-elicited Ca2+ mobilization and cGMP generation were reduced to 40 and 15% after pretreatment with 10 microM 5-HT for 4 hours. NMMA did not modify 5-HT-induced desensitization of either Ca2+ mobilization or cGMP generation, suggesting that NO pathway is independent of the desensitization. The present study has demonstrated the nature of 5-HT-2 receptor-mediated cGMP generation in C6 glioma cells.

Animals↗
PubMed1995

Serotonin-induced platelet calcium mobilization is enhanced in mania.

The time-course of 5-HT-induced intracellular Ca2+ mobilization in platelets displays biphasic curves; a rapid peak occurs within 10 sec, followed by a prolonged plateau phase. In platelets of patients with affective disorders, many reports have suggested that there is an increase in the rapid peak in intracellular Ca2+ mobilization, but there is no report concerning the plateau phase in intracellular Ca2+ mobilization. We, then, assessed the time course of 5-HT-induced Ca2+ mobilization to compare untreated manic patients with euthymic bipolar disorders and normal subjects. Not only peak amplitude but also plateau phase were more significantly enhanced in the platelets of untreated manic patients than in those of normal controls. These results suggest that the serotonergic neural transmission by means of intracellular Ca2+ was enhanced by the prolonged plateau phase as well as by increased peak amplitude in platelets of mania. The enhanced rapid peak and plateau phase in untreated bipolar mania were restored to their control levels in treated euthymic bipolar disorders. These findings suggest that the reduction of the enhancement in Ca2+ mobilization might be related to either the effects of chronic treatment with lithium or the affective states of the patients.

Adult↗
PubMed1995

Inhibitory effects of lithium ion on intracellular Ca2+ mobilization in the rat hippocampal slices.

Lithium is well established as a treatment of manic-depressive illness. As for the mechanism of action of lithium, it is proposed that lithium has effects on intracellular calcium ion (Ca2+) movement. But there are few reports in which the effects of lithium on intracellular Ca2+ movement are observed in the mammalian brain. We therefore examined the effects of lithium on intracellular Ca2+ changes in the rat hippocampal slices with a Ca2+ sensitive dye fura-2, and analyzed by means of a fluorescence microscope, a video-camera and photometrical devices. From the results of treatment with various noradrenergic agonists or antagonists, noradrenaline (NA)-induced intracellular Ca2+ change appears to be mainly mediated by alpha 1-adrenoceptors (AR) rather than alpha 2- or beta-AR. Furthermore, they are considered to be mediated by both alpha 1A-AR and alpha 1B-AR, and to be partly dependent on extracellular Ca2+. Lithium decreased NA-induced intracellular Ca2+ mobilization by attenuation of T1/2 rather than a change in the peak value, and antagonized ouabain-induced intracellular Ca2+ increase. Lithium may therefore suppress intracellular Ca2+ movement by enhancing the extrusion of intracellular Ca2+.

Animals↗
PubMed1995

TJS-010, a new prescription of oriental medicine, antagonizes tetrabenazine-induced suppression of spontaneous locomotor activity in rats.

1. The authors have determined the effect of TJS-010, a new prescription of oriental medicine, on the locomotor activity in rats. 2. Tetrabenazine(TBZ) decreased the spontaneous locomotion in rats, and attenuated the contents of amines and increased their metabolism in various regions in rat brain. 3. TJS-010 inhibited the locomotor suppression induced by TBZ: however, neither amine contents nor their metabolism was not altered, which suggested that TJS-010 postsynaptically modulated the transmission or transduction. 4. Imipramine also inhibited the decrease in locomotion induced by TBZ. 5. These results suggest a possibility that TJS-010 has an antidepressive effect.

Animals↗
PubMed1995

Single or repeated treatment with electroconvulsive shock increases number of serotonin uptake binding sites in the frontal cortex.

The effects of a single or repeated treatment with electroconvulsive shock (ECS) or imipramine on the central serotonin (5-HT) uptake binding sites were studied in the rat frontal cortex and hippocampus. The selective 5-HT uptake inhibitor citalopram and clomipramine potently inhibited the binding for [3H]paroxetine (5-HT uptake binding sites) in the frontal cortex. The antidepressant drugs imipramine and desipramine inhibited the binding moderately, but the 5-HT-related agents, 5-HT, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), mianserin and ketanserin inhibited it weakly. A single ECS increased the density of [3H]paroxetine binding sites, but did not alter the affinity, after 1 or 24 h, in the frontal cortex. Repeated treatment with ECS, but not with imipramine, increased the density of [3H]paroxetine binding sites in the same region. The hippocampal [3H]paroxetine binding did not change after any of these treatments. These results suggest that a single treatment with ECS causes a rapid increase in the neuronal 5-HT transporter complex and the increase lasts for 14 days in the frontal cortex.

Animals↗
PubMed1995

Effect of acute treatment with sodium valproate on catecholamine and serotonin synthesis in mouse cerebral cortex.

We examined the effect of sodium valproate (VPA) on monoamine synthesis in the mouse cerebral cortex by measuring the accumulation of L-3,4-dihydroxyphenylalanine and 5-hydroxytryptophan following inhibition of aromatic L-amino acid decarboxylase. Treatment with VPA decreased catecholamine synthesis, in a dose-dependent manner, with maximum inhibition 60 min following treatment. Muscimol, a GABAA receptor agonist, also decreased catecholamine synthesis, although baclofen, a GABAB receptor agonist, did not. Picrotoxin, a GABAA receptor antagonist, inhibited the VPA-induced decrease in catecholamine synthesis. However, serotonin synthesis was not significantly changed by VPA. These results suggest that acute treatment with VPA reduces the synthesis of catecholamines via GABAA receptors.

Animals↗
PubMed1995

Modulation by sigma ligands of intracellular free Ca++ mobilization by N-methyl-D-aspartate in primary culture of rat frontal cortical neurons.

Despite substantial data on radioligand binding to the sigma receptor, neither the physiologic function nor the intracellular mechanism of this receptor is known. In this study, we examined the effect of sigma ligands on Ca++ influx induced by N-methyl-D-aspartate (NMDA) in single primary cultured rat frontal cortical neurons with fluorescence video microscopy. All sigma ligands tested reduced the NMDA-induced increase in intracellular Ca++ concentration ([Ca++]i) in a dose-dependent manner with IC50 values in the low micromolar range. Inhibition by haloperidol and (+)-N-cyclopropylmethyl-N-methyl-1,4-diphenyl-1-ethyl-but-3-en-1-ylam ine hydrochloride (JO1784) was noncompetitive; but, exogenous glycine (100 microM) did not alter their IC50 values. In addition, haloperidol (1 microM) enhanced Mg+(+)-mediated inhibition of the NMDA-induced [Ca++]i increase (IC50 = 0.45 +/- 0.01 mM vs. an IC50 = 0.98 +/- 0.06 mM for Mg++ alone). Selective sigma receptor ligands (JO1784, (+)-pentazocine) caused a greater reduction of the sustained phase of the Ca++ response to NMDA, whereas haloperidol and DTG reduced both the initial and sustained phase of the response to a similar degree. The rank order of potencies for inhibition of both the sustained Ca++ response phase and (+)-[3H]SKF-10047 binding (Roman et al., J. Pharm. Pharmacol. 42: 439-440, 1989) were similar. These findings suggest that sigma 1 ligands indirectly modulate NMDA receptor complex function through sigma 1 receptors and that sigma ligands facilitate the desensitization of the Ca++ response to NMDA.

Animals↗
PubMed1994

The effect of repeated administration of methamphetamine on dopamine uptake sites in rat striatum.

In this experiment, rats were injected intraperitoneally with 6 mg/kg methamphetamine (MAP) hydrochloride or the same volume of saline once daily for 14 days. Rats were decapitated after a 1-day, 4-day or 10-day withdrawal period. The number and affinity of [3H]mazindol binding sites in the striatum were measured. Their number in the MAP group decreased as compared with controls after a 1-day withdrawal period, but returned to the control level after a 4-day and 10-day withdrawal period. These results are believed to show that the decrease in dopamine uptake sites after repeated administration of MAP is transient and does not contribute to MAP-induced behavioral sensitization.

3,4-Dihydroxyphenylacetic Acid↗