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Biomedical subjects

K Shibata

Publications and source records attributed to K Shibata.

At least 595 records · Page 33Linked to original sources
PubMed1987

Differential mechanisms involved in the anticonflict action of benzodiazepines injected into the central amygdala and mammillary body.

The present study was designed to clarify the mechanism of action of benzodiazepines (BDZ) injected into the central amygdala (ACE) and mammillary body (MB). When gamma-aminobutyric acid (GABA) at doses of 30 and 70 micrograms, muscimol (0.01 and 0.03 microgram), valproate (200 micrograms), atropine (20 micrograms) and cyproheptadine (3 micrograms) were bilaterally injected into ACE, a significant and marked increase in the punished responses of conflict schedule was observed. These drugs injected into MB failed to increase the punished responses. In MB, only noradrenaline (NA, 20 micrograms) showed the anticonflict action. NA 20 micrograms also produced the anticonflict action in ACE. These results suggest that the mechanism of anticonflict action of BDZ is different in brain areas. The GABA-ergic, cholinergic, serotonergic and NA-ergic systems seem to be involved in the mechanism of anticonflict action of BDZ in ACE. While the NA-ergic system appears to be operative in MB.

Amygdala↗
PubMed1987

A comparative study of the calcification-promoting action of 1,25 (OH)2D3 and calcitonin on the growth cartilage of rats with 1-hydroxyethylidene-1, 1-biphosphonic acid (HEBP)-induced rickets.

When HEBP (1-hydroxyethylidene-1, 1-biphosphonic acid) was administered to young rats in large doses over a short period rickets was consistently produced. When HEBP was administered concomitantly with 1,25 (OH)2D3 or calcitonin (CT), calcification appeared in the growth-plate cartilage where there had been an increase in thickness due to the inhibition of calcification. This experiment was done in an attempt to clarify differences in the calcification-promoting mechanisms of 1,25 (OH)2D3 and CT. The serum alkaline phosphatase level was reduced in rats with an accelerated calcification following the administration of 1,25 (OH)2D3, but there was no reduction in the serum alkaline phosphatase level in rats in which the calcification was accelerated by the administration of CT. The mode of appearance of calcification in the growth-plate cartilage by 1,25 (OH)2D3 or CT differed, depending on the time of administration. These results suggest that mechanisms involved in the enhancement of calcification by 1,25 (OH)2D3 and CT differ in cases where rickets are induced by HEBP.

Alkaline Phosphatase↗
PubMed1987

Possible neuronal mechanisms involved in neurotensin-induced catalepsy in mice.

The neuronal mechanisms of neurotensin (NT)-induced catalepsy were investigated in mice. NT administered intracerebroventricularly (ICV 0.5, 1.0 and 2.0 micrograms) produced catalepsy in a dose-dependent fashion. A significant effect was observed at 2.0 micrograms and a maximal effect 2-3 h after injection. The NT-induced catalepsy was inhibited by pretreatment with atropine, trihexyphenidyl or biperiden (each drug, 0.8-5.0 mg/kg, IP), anticholinergic drugs, and L-DOPA (100, 200 mg/kg, IP). However, the catalepsy was not significantly antagonized by p-chlorphenylalanine (300 mg/kg X 3 days, IP) or methysergide (5, 10 mg/kg, IP), antiserotonergic drugs, and was not potentiated by the GABAergic drugs, aminooxyacetic acid (25 mg/kg, IP) or muscimol (1 mg/kg, IP). In addition, the NT-induced catalepsy was dose-dependently reduced by antihistamines, such as diphenhydramine (0.8-10 mg/kg, IP) and tripelennamine (0.4-5.0 mg/kg, IP) and was potentiated after treatment with histidine (250, 500 mg/kg, IP), a precursor of brain histamine. NT-induced catalepsy was also reduced by ICV pretreatment with diphenhydramine (1-5 micrograms/rat), a H1 antagonist, but not by cimetidine (5, 20 micrograms/rat), a H2 antagonist. These findings suggest that the catalepsy induced by NT may involve not only central cholinergic and dopaminergic mechanisms but also a histaminergic mechanism mediated via H1-histamine receptors, and seems to differ from the catalepsy induced by neuroleptics.

Animals↗
PubMed1987

Killing of preimplantation mouse embryos by main ingredients of cleansers AS and LAS.

When main ingredients of cleansers, alcohol sulfate (AS) and linear alkylbenzene sulfonate (LAS), were applied to the dorsal skin of pregnant JCL:ICR mice during preimplantation period (days 0-2), significant numbers of embryos collected from the oviducts and uteri on day 3 showed severe deformity or remained at the morula stage. Most of abnormal embryos were fragmented or remained at the 1-8 cell stages, and they were either dead or dying. Even when these abnormal embryos were cultivated in the detergent-free medium, they were not recovered, while most growth-retarded embryos (morula) could grow and hatch with one or two days lag by the further in vitro cultivation. Similar results were observed with commercially obtained kitchen detergent and hair shampoo, although such embryocidal effects were not detected with natural soap and distilled water. Fertilized eggs may be specifically sensitive to synthetic detergents. Very low doses of X-rays also induced significant yields of abnormal embryos. Major difference between X-rays and detergents was that X-ray-induced abnormality appeared at the morula or blastocyst stage, while detergent-induced one did at the earlier stages.

Alcohols↗
PubMed1987

Promotion of hepatocarcinogenesis by suxibuzone in rats initiated with 3'-methyl-4-dimethylaminoazobenzene.

Among phenylbutazone (PZ) and its related compounds, suxibuzone (SUX) caused the most extensive decrease in pyruvate kinase (PK) activity with lower toxicity. Therefore, we studied the effect of SUX on rat hepatocarcinogenesis to confirm our assumption that an agent which causes a prolonged decrease in PK activity in rat liver promotes hepatocarcinogenesis. For initiation rats were fed a diet containing 0.06% 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB) for 4 weeks. At the end of 53 weeks of the experiment the incidences of liver tumors were 14.3 and 70.0% in the rats fed basal diet and in the rats fed 0.5% SUX diet, respectively, after the initiation. No tumors were observed in rats fed the SUX diet without the initiation. The result shows that SUX promotes hepatocarcinogenesis and supports the above assumption.

Administration, Oral↗
PubMed1987

Production of immunoglobulin M (IgM) autoantibodies to IgG in rabbits inoculated with Mycoplasma salivarium cells grown in medium supplemented with rabbit serum.

Mycoplasma salivarium cells propagated in PPLO broth (Difco Laboratories, Detroit, Mich.) supplemented with rabbit serum (10% [vol/vol]) and harvested by centrifugation were shown to contain rabbit immunoglobulin G (IgG) (approximately 4 to 10% of total cell proteins) and to produce IgM autoantibodies to IgG when inoculated into rabbits.

Animals↗
PubMed1987

Purification and characterization of an aminopeptidase from Mycoplasma salivarium.

The aminopeptidase which had been shown to be present in Mycoplasma salivarium was found to be associated with the cell membranes of the organism. The enzyme was solubilized in water by papain digestion of the membranes pretreated with Triton X-100 and purified approximately 130-fold by ion-exchange chromatography on DEAE-Sephadex A-50, affinity chromatography on L-leucylglycine-AH-Sepharose 4B, and gel filtration on Sepharose CL-6B. The purified enzyme had a molecular mass of 397 kilodaltons, estimated by gel filtration through Sepharose CL-6B, and gave two bands of activity in analytical disc polyacrylamide gel electrophoresis: a dense, diffuse band and a less dense, narrow one, accounting for 90 and 5% of stained proteins in the gel, respectively. The purified protein revealed two bands with molecular masses of 50 and 46 kilodaltons by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The enzyme catalyzed selectively the cleavage of the N-terminal arginine and leucine residues of peptides; had a pH optimum at 8.5; and was inhibited remarkably by bestatin, o-phenanthroline, EDTA, and L-cysteine, but was activated nine- and twofold by MnCl2 and MgCl2, respectively. The enzyme pretreated with MnCl2 had much higher maximum velocity (Vmax) for L-leucine-p-nitroanilide than the one not treated. That is, the Michaelis constant (Km) and Vmax values of the pretreated enzyme were 10.5 mM and 12.1 microM/min, respectively, whereas those of the untreated enzyme were 5.8 mM and 1.6 microM/min, respectively.

Aminopeptidases↗
PubMed1987

Inhibition of hypertension and salt intake by oral taurine treatment in hypertensive rats.

Effects of oral treatment with taurine on fluid intakes produced by renin were assessed in spontaneously hypertensive rats of the Okamoto strain (SHR). Renin injected into the preoptic area increased water intake and evoked salt (2.7% NaCl solution) intake, and angiotensin II injected into this area increased water intake, but not salt intake, in both SHR and control normotensive Wistar-Kyoto rats (WKY). The salt intake elicited by renin, but not water intake produced by renin or angiotensin II, was potentiated in SHR. These effects of renin and angiotensin II on fluid intakes were antagonized by previous administration of taurine or gamma-aminobutyric acid into the cerebral ventricles in both strains. When SHR received water containing 3% taurine from 32 to 105 days of age, development of hypertension was inhibited. Renin administered into the preoptic area at 105 days of age caused an increase in salt intake, but the increase was markedly inhibited by the oral administration of taurine as well. These results show that salt appetite produced by centrally administered renin is exaggerated in SHR and that development of hypertension as well as renin-induced salt appetite in SHR is inhibited by dietary taurine.

Administration, Oral↗
PubMed1987

The metabolism of roxatidine acetate hydrochloride in rat and dog liver homogenates.

The metabolites were identified by gas chromatography-mass spectrometry (GC-MS). When an equimolar mixture of roxatidine acetate hydrochloride and its deuterated compound, labeled with ten deuterium atoms in the piperidine ring, was incubated with the 9000 X g supernatant (S-9) fraction of either rat or dog liver homogenate, the oxygenated metabolites of the piperidine ring such as the 3-hydroxypiperidine derivative (M1) and the 2-oxopiperidine derivative (M2) were isolated from rats but M2 was not isolated from dogs. These results suggested that the species differences in the metabolism of the piperidine ring in vitro are similar to that in vivo. The deuterium isotope effect (H/D) was 1.34 for M1 and 1.47 for M2 in rats, while the value for M1 in dogs was 1.69. On the other hand, the formation of these oxidative metabolites was inhibited by carbon monoxide in incubations using hepatic microsomes, suggesting that the reaction was catalyzed by cytochromes P-450.

Animals↗
PubMed1987

Behavioral and electroencephalographic effects of zopiclone, a cyclopyrrolone derivative.

Behavioral effects of zopiclone were investigated in mice and rats and compared with the data on diazepam, nitrazepam and flurazepam. The electroencephalographic effect of the drug was also examined in unanesthetized rabbits with chronic electrode implants and compared with that of diazepam. The present results indicate that zopiclone possesses pharmacological properties qualitatively similar to benzodiazepines, which are characterized by potent anticonflict and antiaggressive effects and much weaker anticonvulsant, muscle relaxant, ataxiogenic, sedative and anesthesia potentiating effects; the properties of this drug were compared with those of diazepam, nitrazepam and flurazepam. Zopiclone suppressed the EEG arousal responses and inhibited afterdischarges induced by electrical stimulation of the hippocampus and amygdala. The effects of zopiclone on EEG and afterdischarges were approximately 1/10 those of diazepam.

5-Hydroxytryptophan↗
PubMed1987

The inhibitory effects of calmodulin antagonists on TSH-stimulated thyroid hormone release by mouse thyroid lobes.

Calcium ions have been shown to play a mojor regulatory role in the release of various hormones from a wide variety of endocrine organs. More recently, in vitro evidence suggests that a calcium-binding protein, calmodulin, is also involved in the release of many hormones. So we examined the effects of several types of calmodulin antagonists on TSH-stimulated thyroid hormone release in vitro. Mouse thyroid lobes (one thyro-tracheal unit/tube) were incubated in Krebs-Ringer bicarbonate buffer at 37 degrees C for 4h. Free thyroxine (fT4) released in the incubation medium, thyroidal cAMP and calmodulin content were measured by RIA. TSH (5 mU/ml) and dibutyryl cAMP (DBC) (200 micrograms/ml) caused a 2-4 fold increase in thyroidal release of fT4. The stimulatory effects of TSH on fT4 release were significantly inhibited by trifluoprazine and prenylamine lactate at the concentration of 5 X 10(-5) M. More specific calmodulin antagonists, W-7 and W-13, were also shown to inhibit TSH stimulation of fT4 release at the concentration of 5 X 10(-5) M. In contrast, TSH stimulation of fT4 release was not depressed by non-specific antagonists, W-5 or W-12, at the same concentration as 5 X 10(-5) M. Further, W-13 also markedly inhibited DBC-stimulated fT4 release. Neither TSH nor PGI2 altered the thyroidal calmodulin content, dissociating with a marked increase in the cAMP concentration. These results suggest that calmodulin plays an important role in TSH-stimulated thyroid hormone release and further that this mechanism exists, at least in part, at the site subsequent to the generation of cAMP.

Animals↗