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Biomedical subjects

K Moroi

Publications and source records attributed to K Moroi.

At least 37 records · Page 2Linked to original sources
PubMed1992

Localization of a 82 kDa protein in postsynaptic density and its association with cytoskeletons.

A fraction of synaptic junctional complex (SJC) was prepared from rat synaptosomes and served as antigen material to produce monoclonal antibodies (Mab) for examining the component proteins of the SJC. An antibody, Mab SJ-8, was obtained, which recognized a protein with a molecular weight of 82,000 Da in the SJC preparation by immunoblot analysis. The immunohistochemical localization of the 82 kDa protein was studied with the rat cerebellum. Mab SJ-8 labeled the peripheral areas of the Purkinje and granule cells. Small punctate areas were also stained in the molecular layer with SJ-8. Intracellular localization of the protein was examined with rat brain synaptosomes. Immunoelectron microscopy demonstrated that Mab SJ-8 strongly labeled the postsynaptic density (PSD) and also a fibrous network spreading out of it. However, the antibody did not label the pre- or post-synaptic membrane or the cleft material.

Animals↗
PubMed1991

Fetal death associated with measles virus infection of the placenta.

A case of fetal death at 25 weeks' gestation, which was associated with maternal measles infection, is described. Immunohistochemical study revealed measles virus antigen in the syncytial trophoblastic cells and decidua but not in the fetus. Results suggest that fetal death was caused by measles virus infection in the placenta. As far as we know, this is the first report in which a measles virus antigen was detected in the placenta by the immunohistochemical method.

Adult↗
PubMed1991

Bovine brain coated vesicles contain guanine nucleotide regulatory proteins.

Binding of [3H]guanosine triphosphate (GTP) with a high affinity was found to be present in the coated vesicle fraction prepared from bovine cerebral cortex. The binding was saturable and displaced by 1 microM of GTP, guanosine diphosphate and guanosine 5'-(3-O-thio)triphosphate. Incubation of the vesicles with islet-activating protein and [32P]NAD resulted in ADP-ribosylation of a 39,000-41,000-dalton polypeptide. Antibodies to the alpha-subunit of stimulatory guanine nucleotide regulatory proteins (G-proteins) immunoblotted 52,000- and 45,000-dalton polypeptides. The results indicated that stimulatory and inhibitory G-proteins are contained in a fraction of the bovine brain coated vesicles.

Adenosine Diphosphate Ribose↗
PubMed1989

Detection and characterization of 3H-clonidine binding sites in coated vesicles isolated from bovine brain.

The binding of 3H-clonidine to bovine brain coated vesicles was studied. The binding was reversible and saturable. Saturation studies revealed a one-site interaction: Kd was 8.7 nM and Bmax was 24.5 fmol/mg protein. Noradrenaline, yohimbine and phenoxybenzamine displaced 3H-clonidine binding from the binding sites at concentrations of 10(-7)-10(-4) M. The results indicate that the coated vesicles from the bovine cerebral cortex contain 3H-clonidine binding sites comparable to the low affinity sites of alpha 2-adrenergic receptors in bovine brain membranes.

Adrenergic alpha-Agonists↗
PubMed1988

Involvement of GABAergic systems and benzodiazepine receptors in the jumping behavior induced by harmine and apomorphine in rats.

Harmine (HA) induces a jumping behavior in rats when the central dopaminergic function has been activated. Possible involvement of the GABAergic systems and the benzodiazepine receptors (BZA-R) in the jumping behavior induced by HA and apomorphine (APO) was investigated. Pretreatment with GABAergic agonists, muscimol (0.05-0.2 mg/kg) and diazepam (0.2-1.0 mg/kg), and antagonists, picrotoxin (0.1-0.5 mg/kg) and bicuculline (0.1-0.5 mg/kg), suppressed the jumping behavior in a dose-dependent manner in rats treated with HA (10 mg/kg) and APO (2 mg/kg). After treatment with 2, 5 or 10 mg/kg of HA in combination with 2 mg/kg of APO, a decrease in 3H-diazepam binding to the brain regional membranes was observed in the corpus striatum (CS) in a dose-dependent manner, but not in the other brain regions. The decrease in the 3H-diazepam binding to the CS membranes was proportional to the increase in the HA levels in the CS, and the HA levels were correlated with the intensity of jumping behavior. Pretreatment with Ro 15-1788, an antagonist of BZA-R, suppressed the jumping behavior induced by HA and APO. These results indicated the involvement of the GABAergic systems in the jumping behavior and suggested that HA induced the jumping behavior partly as a result of interacting with the BZA-R.

Alkaloids↗
PubMed1987

Monoclonal antibodies to a brain dopamine binding protein: production, specificity, and immunohistochemistry.

A dopamine binding protein (DABP) has been purified from the rat brain synaptic membrane to homogeneity by affinity chromatography and gel electrophoresis. The monoclonal antibodies against the DABP were produced by the mouse-mouse hybridoma technique and characterized for their specificity to dopamine receptors by displacement of dopamine receptor binding. These monoclonal antibodies have been used to localize DABP in rat brain by immunohistochemistry. A specific linear structure of reaction product was seen in both caudate nucleus and cerebral cortex. This finding suggests that the DABP is present in the cerebral cortex and caudate nucleus as a membranous component of the neurons or their processes.

Animals↗
PubMed1987

Estimation of harmine and its derivatives by HPLC: correlation of brain harmine levels with jumping behavior in rats.

Brain harmine was simply and sensitively determined by high performance liquid chromatography (HPLC), and the relationship between brain harmine concentrations and the jumping behavior induced by harmine and apomorphine was investigated. The concentration of harmine and the peak height in HPLC showed a good correlation, and the detection limit was 0.05 pmole harmine. In rats treated with 2, 5 and 10 mg/kg of harmine, the concentrations of harmine in the brain cortex were 9.0, 21.3 and 43.1 nmole/g tissue (wet wt.), respectively. The regional brain harmine concentrations and the jumping activity measuring by a scoring system increased with increasing doses of harmine administered, and there was a direct relation between the harmine concentrations and the jumping activity. This relation was observed in washed membranes in which about 40% of the harmine in whole homogenate was present. Tissue subfractionation showed that 30% of the harmine in whole brain homogenates was in the P2 fraction, and of this, 70% was located in the synaptosomes. The brain homogenate did not metabolize harmine and no metabolite was detected in the brain 10 min after treatment with harmine and apomorphine. These results suggest that harmine itself, but not its metabolites, may be responsible for inducing the jumping behavior and that the jumping activity is correlated with brain harmine concentrations.

Alkaloids↗
PubMed1985

Effects of phospholipids on the specific binding of [3H]spiroperidol to the cholate extract of rat brain synaptic membranes.

Effects of phospholipids including PC, PE, PI, and PS on the specific [3H]SPD binding to the solubilized dopamine receptors were examined in the cholate extracts of the cortical and striatal synaptic membranes (P2M) of the rat brain. PC and PS, but not PE or PI, at 0.4 mM greatly enhanced the specific [3H]SPD binding to the cholate extracts of both cortical and striatal P2M fractions. PC and PS did not enhance the specific [3H]DA binding to the same cholate extracts. The enhancing effects of PC and PS were temperature-dependent and in a dose-response manner peaking at 0.4 mM and 0.2 mM respectively. Such temperature dependence indicated that the PC effects were not due to trapping of [3H]SPD by PC but represented a possible DAR-PC complex formation that allowed higher binding for the ligand. Failure of natural cerebellar P2M in enhancing the [3H]SPD binding to the cholate extract supports the notion that fluidity of the phospholipids is required for the binding or the formation of the DAR-PC (or PS) complex. Scatchard analysis of the [3H]SPD binding to the cholate extract in the absence or presence of PC or PS indicated that the PC or PS enhancement of the ligand binding may be mainly due to an increase in the number of binding sites since both PC and PS significantly increased the Bmax but not the Kd of the binding.

Animals↗
PubMed1985

Reduction of ochratoxin A toxicity in mice treated with phenylalanine and phenobarbital.

LD50 of ochratoxin A (OCT A) was estimated to be 29.4 mg/kg in intraperitoneal (i.p.) and 46.0 mg/kg in per os (p.o.) administration in ddY strain male mice. Acute toxicity of OCT A was reduced by simultaneous administration of phenylalanine or by pretreatment with phenobarbital (PB) for 1 week and the LD50 increased to 1.5-2.0 times control. Chromatographic analyses of OCT A and the metabolite, OCT alpha, extracted from urine and bile after administration of OCT A, indicated that amounts of OCT A and OCT alpha decreased in the urine and increased in the bile of PB-pretreated mice, suggesting that a change in metabolism of OCT A could cause the decrease in the toxicity of OCT A in PB-pretreated mice.

Animals↗
PubMed1985

[Loneliness and self-consciousness in high-school students].

To examine relationships between loneliness and various aspects of self-consciousness in high-school students, UCLA Loneliness Scale (Russell, Peplau, & Cutrona, 1980), Self-Esteem Scale (Rosenberg, 1979), Self-Consciousness Scale (Fenigstein, Scheier, & Buss, 1975), Self-Monitoring Scale (Synder, 1974), and a High-School Life Questionnaire were administered to the first grade students in a high school (N = 182). Loneliness (alpha = .885), higher for males than for females, was significantly correlated with various aspects of their high-school lives. Loneliness was negatively correlated with self-esteem and self-monitoring, and was positively correlated with social anxiety. Only for males, a positive correlation was obtained between loneliness and private self-consciousness. Discriminant analysis and other correlational analyses also suggested that loneliness in males was related to various aspects of self-consciousness.

Adolescent↗
PubMed1984

A brain synaptic dopamine-binding protein: isolation and partial characterization.

A dopamine-binding protein (DABP) has been purified from the rat brain cortex to homogeneity. Solubilization of the DABP from the synaptosomal membranes (P2M) by cholic acid, subsequent agarose gel filtration of the cholic acid extract to separate phospholipids from the DABP, and lastly DA affinity chromatography successfully resulted in a purified DABP with approximately 0.006% yield in protein concentration and 0.03% yield in specific [3H]-DA binding. The specific [3H]-DA binding of the purified DABP was 117 fmol/mg protein/10 min with a 4.6-fold purification compared with the whole homogenate. The purified DABP had an Rf value of 0.67 on native disk polyacrylamide gel and it gave one single polypeptide subunit on the SDS gel with an Rf value of 0.63. The apparent molecular weight of this single subunit was estimated to be 34.5 kilodaltons. The elution patterns from either DA- or ADTN-affinity (2-amino-6,7-dihydroxy-1,2,3,4-tetrahydronaphthalene-affinity) columns indicated that this DABP had higher affinity for DA agonists than for DA antagonists. Photoaffinity labeling of [3H]-DA to this DABP in the P2M fraction and the specific [3H]-DA to the purified DABP demonstrated a nanomolar range affinity corresponding to either D2 or D3 receptors. These data suggested that the purified DABP could be related to either D2 or D3 receptors in the brain.

Animals↗
PubMed1982

Inhibitory effect of leptophos on carboxylesterase (isocarboxazid amidase) in rat liver.

The organophosphate insecticide, leptophos, inhibited rat liver isocarboxazid amidase (ISOCase) activity to 20% of control at 5.0 mg/kg l h after administration, but at this dose brain cholinesterase (ChE) activity was not affected. The activity of ISOCase decreased to 29 and 0% of control 24 h after treatment with leptophos at doses of 2.5 and 5.0 mg/kg, respectively. With repeated administration of leptophos at a dose of 1 mg/kg for 10 days, ISOCase activity decreased to 34% of control on day 1 and the inhibition increased to 85% on day 10 without inhibition of brain ChE activity. After cessation of three successive daily doses (1 mg/kg/day), the ISOCase activity was gradually restored near to control levels in 8 days. Pretreatment with carboxylesterase inhibitors, triorthocresylphosphate (TOCP) and bis-p-nitrophenylphosphate (BNPP), potentiated the inhibition of brain ChE by leptophos, suggesting that ISOCase might take a role in leptophos detoxification.

Animals↗
PubMed1982

Dual effects of tetrachlorvinphos on procaine toxicity and procainesterase activity in rats.

The effect of tetrachlorvinphos (TCVP) on liver procainesterase (PROCase) and procaine toxicity was studied in rats. TCVP is an organophosphate with an inducible effect on drug metabolizing enzymes. A single oral dose of 500 mg/kg of TCVP caused a remarkable decrease in PROCase (40% of control) 24 hr later and increased the motality after injection of procaine (250 mg/kg, i.p.) from 54% to 87%. Conversely, it was observed that PROCase elevated to 140% of the control and mortality decreased from 54% to 25% on day 3. With repeated administration of TCVP (500 mg/kg/day) for 5 days, the PROCase activity that was inhibited on day 1 was gradually restored to normal levels by 5 days and the mortality altered to 25%. The inducible effect on PROCase was examined using desmethyl-TCVP, a metabolite of TCVP without inhibitory effect on the enzyme; PROCase activity was enhanced to 1.6-fold of the control and procaine concentration in the brain was reduced to 30% of the control, accompanied with no death of rats after procaine injection. Electrophoresis of the solubilized liver microsomal fraction confirmed the inducible effect of TCVP on PROCase; microsomal protein from the TCVP-treated rat was more deeply stained than that from the control, and the PROCase activity of two anodic bands increased in the TCVP-treated microsomes. These results indicate that TCVP has a dual action on PROCase, inducible and inhibitory, and that the direct inhibitory effect of TCVP might mask the increased amount of the enzyme induced by repeated administration of TCVP. The dual effect of TCVP on PROCase would cause the change in procaine toxicity.

Animals↗
PubMed1979

Partial purification and immunological aspects of carboxylesterase from rat liver microsomes.

Carboxylesterase (CEase) was solubilized from rat liver microsomes by autolysis followed by cholate treatment and then purified by the combination of ammonium sulfate fractionation, gel filtration, chromatography on DEAE Sephadex A-50 and hydroxyapatite and preparative Disc electrophoresis. The overall purification was 25-fold with a yield of 6% of the original enzyme activity. Analytical Disc electrophoresis of the final enzyme preparation showed a single band. However, SDS polyacrylamide gel electrophoresis revealed one main band of 93% and three other minor bands. To investigate the interaction between CEases of rat, monkey, pig and rabbit liver microsomes, rabbit antibody to the above enzyme preparation was prepared and immunological analyses, i.e., Ouchterlony's test and immunoelectrophoresis, were performed. In the comparative double diffusion test, the partial fusion of precipitation line between anti-rat CEase and the enzymes of other species was observed. In the second analysis, sharp arc precipitation lines also could be seen in all specimens and, furthermore, mobilities of each enzyme were different. These observations suggest that rat liver CEase seems to be immunologically related in part but not completely identical with the CEases of other species and the charge difference may exist in these specimens.

Animals↗
PubMed1977

Effect of pretreatment with tricresylphosphates and phenobarbital on the metabolism and toxicity of procaine in rats.

We examined the effects of pretreatment with phenobarbital and tricresylphosphates, TOCP and TCP, on the metabolism and toxicity of procaine in rats. A single administration of procaine at a dose of 250 mg/kg intraperitoneally to adult rats caused convulsion, however, phenobarbital (80 mg/kg intraperitoneally daily, 4 days) pretreatment protected against the toxicity or procaine. In contrast, pretreatment of rats with TOCP (10 mg/kg per os) or TCP (10 mg/kg per os) revealed a higher incidence of toxicity as compared to control rats. Mortality in procaine-treated rats was significantly decreased with phenobarbital-pretreatment and, conversely, increased with TOCP and TCP. Paralysis, convulsion and death were induced at the brain level of procaine of 0.303 +/- 0.025, 0.480 +/- 0.026 and 0.565 +/- 0.018 mumole/g brain wet weight, respectively. Toxic effects of procaine were, therefore, concluded to be due to the accumulation of the drug in the brain.

4-Aminobenzoic Acid↗