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H Yokoo

Publications and source records attributed to H Yokoo.

At least 73 records · Page 4Linked to original sources
PubMed1996

ATP-sensitive K+ channel openers block sulpiride-induced dopamine release in the rat striatum.

In vivo brain microdialysis was used to investigate the role of ATP-sensitive K+ (KATP) channel openers in dopamine release regulated by dopamine autoreceptors in the rat striatum. Local infusion of two KATP channel openers, nicorandil (10(-5)-10(-3) M) and cromakalim (10(-5)-10(-3) M), into the striatum thorough the dialysis membrane produced dose-dependent decreases in extracellular concentrations of dopamine. Local application of the dopamine D2 receptor antagonist, (-)-sulpiride (10(-5) M), produced significant increases in extracellular concentrations of dopamine. Both nicrorandil (10(-5) M) and cromakalim (10(-4) M) blocked significantly (-)-sulpiride (10(-5) M)-induced increases in dopamine levels in the striatum. These results suggest that activation of KATP channels in the striatum causes decreases in endogenous dopamine release in vivo. Furthermore, the sulpiride-induced increases in dopamine levels caused by blocking the tonic activation of dopamine autoreceptors were inhibited by activation of KATP channel. These data indicate that KATP channels may be present in nigrostriatal dopaminergic terminals and that striatal dopamine autoreceptors inhibit dopamine release tonically by activation of KATP channels.

Adenosine Triphosphate↗
PubMed1996

A monoclonal antibody that recognizes a carbohydrate epitope of human protoplasmic astrocytes.

By hybridizing mouse myeloma cells with spleen cells from a BALB/c mouse immunized with the glial cell-rich fraction prepared from an autopsied human brain, we established a hybridoma that produces a monoclonal antibody to protoplasmic astrocytes (PA). The antibody, named PRAS-1, consistently labeled cytoplasm of PA with a granular pattern. In a few cases, the cytoplasmic processes of several astrocytes in gray and white matter were also stained. The immunoreactivity was lost after periodic acid treatment or methylation, showing that the epitope is composed of a carbohydrate. The cytoplasmic reaction was resistant to protease digestion and lost after incubation in an organic solvent, suggesting that a glycolipid is the antigen. On the other hand, the reaction in the processes disappeared upon protease digestion. Ultrastructurally, the immunoreaction was localized to secondary lysosomes. Cross-reactivity was noted on a small number of incidental neurons, corpora amylacea, hepatocytes and esophageal epithelial cells. A long period of formalin fixation did not deteriorate the antigenicity. PRAS-1 was demonstrated to detect PA immunohistochemically on paraffin sections, and may be applicable to further investigations into development or neoplasms of human astrocytes.

Aged↗
PubMed1996

Up-regulation of functional voltage-dependent sodium channels by insulin in cultured bovine adrenal chromaffin cells.

Treatment of cultured bovine adrenal chromaffin cells with 100 nM insulin raised [3H]saxitoxin ([3H]-STX) binding in a time-dependent manner (t1/2 = 26 h). Insulin (100 nM for 4 days) increased the Bmax of [3H]STX binding by 49% without changing the KD value and also augmented the maximal influx of 22Na+ due to 560 microM veratridine by 39% without altering the EC50 value of veratridine. The stimulatory effect of insulin on 22Na+ influx was concentration-dependent with an EC50 of 3 nM, whereas insulin-like growth factor (IGF)-I had little effect at 1 nM. Ptychodiscus brevis toxin-3 allosterically potentiated veratridine (100 microM)-induced 22Na+ influx by approximately twofold in both insulin-treated cells and untreated cells. Veratridine-induced 45Ca2+ influx via voltage-dependent Ca2+ channels and catecholamine secretion were also enhanced by insulin treatment, whereas insulin did not alter nicotine-induced 22Na+ influx via the nicotinic receptor-ion channel complex and high-K+ (direct activation of voltage-dependent Ca2+ channels)-induced 45Ca2+ influx. Stimulatory effects of insulin on [3H]-STX binding and veratridine-induced 22Na+ influx were nullified by simultaneous treatment with either 5,6-dichlorobenzimidazole riboside, an inhibitor of RNA synthesis, or cycloheximide, an inhibitor of protein synthesis, whereas insulin treatment did not appreciably increase the level of mRNA encoding the Na+ channel alpha-subunit. These results suggest that the binding of insulin to insulin (but not IGF-I) receptors mediates the up-regulation of functional Na+ channel expression at plasma membranes; this up-regulation may be due, at least in part, to the de novo synthesis of an as yet unidentified protein(s).

Adrenal Medulla↗
PubMed1996

A monoclonal antibody that specifically recognizes a novel mitochondrial protein of human astrocytes.

We established a monoclonal antibody to human astrocytes using a human glial cell-rich fraction as the immunogen. The antibody, named PRAS-4, specifically labeled populations of astrocytes in a fine granular manner immunohistochemically. In formalin-fixed, paraffin-embedded tissue sections, PRAS-4-positive astrocytes were extensively distributed in the gray matter of the central nervous system, namely the cerebral cortex, basal ganglia, diencephalon, midbrain, various nuclei of the brain stem, cerebellar cortex and nuclei, and spinal cord. In the white matter, a few positive astrocytes were located mostly in the perivascular area. The reaction was lost after protease digestion and it resisted periodic acid, suggesting that the epitope is of a protein. The molecular weight of the antigen was estimated as 62 kDa. Ultrastructurally, the immunoreaction was localized on the outer and inner membranes of astrocytic mitochondria, and unlabeled mitochondria coexisted in the same cells. Extra-mitochondrial regions were not stained. PRAS-4 preferentially labeled astrocytes of the protoplasmic type, and may be applicable to studies on the development, specific functions and neoplasms of astrocytes.

Adult↗
PubMed1996

[Refractory anemia with excess of blasts (RAEB) with a high level of HbF that preceded apparent pancytopenia].

A 76-year-old male was kept under observation for idiopathic interstitial peumonitis in our hospital from August 1992. Laboratory data revealed a slightly high level of HbF (2.7%) but normal values of other hematological examination. The level of HbF increased slowly, and in April 1994, pancytopenia appeared for the first time. Bone marrow was normocellular with myelodysplasia and 9% blasts. Cytogenetic analysis revealed 46, XY, del (20) (q11;q13). He was diagnosed as having myelodysplastic syndrome (MDS), refractory anemia with excess of blasts. At diagnosis of MDS, the level of HbF was 20.0%. He developed acute myelocytic leukemia 3 months later. It has been reported that approximately 40% of patients with MDS have higher HbF levels than normal, which is considered to be functional abnormality of the MDS clone. It is suggested that the MDS clone had already increased in this patient at presentation, 32 months before pancytopenia appeared.

Aged↗
PubMed1996

[Comparison of analgesic effect of lidocaine tape versus eutectic mixture of lidocaine and tetracaine during infiltration of local anesthetics before epidural block].

We compared analgesic effects of a lidocaine tape (Penles) and the eutectic mixture of lidocaine and tetracaine (LT ointment) during local infiltration before epidural block. Ninety-six patients were randomly assigned to 3 groups. In groups 1 and 2, lidocaine tape was applied on the skin of the epidural puncture site 30-60 min before epidural block. In group 3, 1 g of LT ointment was applied on the same place 1-2 h before block. Additionally, patients in groups 2 and 3 were medicated intramuscularly with midazolam 5 mg. Although no significant difference in pain relief in 5 pin prick tests was observed among the three groups, there was a significantly greater decrease in the pain score during the infiltration of local anesthetics in groups 1 and 2, compared with group 3. There was no significant difference in the pain score between groups 1 and 2. We concluded that lidocaine tape is more useful than LT ointment in decreasing pain of local infiltration anesthesia, and midazolam did not exert any supplementary analgesic effect.

Administration, Topical↗
PubMed1996

Undifferentiated tumor originating in the cerebral dysgenetic lesion resembling fibrous cartilage: case report.

A 33-year-old woman had an undifferentiated tumor originating in the cerebral dysgenetic lesion resembling fibrous cartilage. She had a headache, vomiting, late-onset epilepsy and left hemiparesis. The lesion was located in the right temporal lobe on computed tomographic (CT) scan. It was totally resected and only local irradiation was performed postoperatively. Normal cortical architectures were lost in the resected specimens. Straight or curved fasciculi composed of fine collagen fibers were distributed in parallel and perpendicular to the cortical surface in the mildly eosinophilic hyaline matrix. Hypertrophic astrocytes were scattered with low cellularity in these abnormal cortices. Clusters of tumor cells were observed in a few areas. The tumor cells, having oval and relatively vesicular nuclei with a few prominent nucleoli and basophilic well-circumscribed narrow cytoplasm, had proliferated diffusely with a cobblestone appearance. Immunohistochemical and electron microscopic investigations demonstrated no evidence of specific differentiation, either. There were 14.5 mitotic figures/high power field on average and most nuclei of the tumor cells were strongly positive for proliferating cell nuclear antigen (PCNA). Moreover, subarachnoid dissemination of the tumor cells were apparent in a few areas. Nevertheless the patient returned to work and no recurrence was observed for 10 years postoperatively. We concluded that neoplastic transformation occurred de novo in the dysgenetic cortex.

Adult↗
PubMed1995

A neuronal fibrillary inclusion shares the epitope of p24 of human immunodeficiency virus.

A monoclonal antibody to p24 of human immunodeficiency virus (HIV) was demonstrated to react with degenerated neurons immunohistochemically. In a case of Pick's disease, the neurons of the dentate gyrus were labeled with the antibody, while normal-looking ones and glial components were negative. The positive structures showed argyrophilia by the Bielschowsky and Bodian methods. Antibodies to ubiquitin, paired helical filament and tau did not react with the inclusions. Ultrastructurally, they consisted of skeins of fuzzy-surfaced fibrils with a diameter of 15 nm. In cases of Alzheimer type dementia, thread-like positive profiles were observed in some neurofibrillary tangle-bearing neurons. These studies revealed the cross-reactivity of the anti-HIV p24 antibody to unknown types of neuronal inclusions and provide a new aspect for research into neurodegenerative disorders.

Adolescent↗
PubMed1995

Pyogenic granuloma in Barrett's esophagus mimicking esophageal carcinoma.

A 31-year-old white man with a history of testicular carcinoma and lymphoma developed severe reflux esophagitis with stricture formation requiring repeated dilatation. Barrett's esophagus was histologically confirmed. The Barrett's mucosa was observed endoscopically and became polypoid, mimicking an esophageal carcinoma. The polyp was evaluated by endoscopic ultrasonography and ultrasonically guided aspiration cytology. It was managed by snare cautery removal, which showed a pyogenic granuloma.

Adult↗
PubMed1995

The role of ATP-sensitive potassium channels in striatal dopamine release: an in vivo microdialysis study.

We used in vivo brain microdialysis to investigate the role of adenosine triphosphate (ATP)-sensitive potassium (KATP) channels in dopamine (DA) release regulated by DA autoreceptors in the rat striatum. Local infusions of the KATP channel opener nicorandil (10(-5)-10(-3) M) into the striatum through the dialysis membrane produced dose-dependent decreases in extracellular concentrations of DA. Local application of the D2 receptor antagonist (-)-sulpiride (SLP, 10(-5) M) or the KATP channel blocker quinine (QIN, 10(-3) M) produced significant increases in extracellular concentrations of DA. Nicorandil (10(-3) M) significantly blocked SLP (10(-5) M)- or QIN (10(-3) M)-induced increases in DA levels in the striatum. These results suggest that activation or inhibition of the KATP channel in the striatum causes decreases or increases, respectively, in endogenous DA release in vivo. Furthermore, SLP-induced increases in DA levels caused by blocking the tonic activation of DA autoreceptors are inhibited by the activation of KATP channels. These data suggest that striatal DA autoreceptors may inhibit DA release tonically by activating the KATP channel.

Adenosine Triphosphate↗
PubMed1995

Lipopeliosis.

Explore the source record for details and available documents.

Fatty Liver↗
PubMed1995

Differential effects of dopamine antagonists on evoked dopamine release from slices of striatum and nucleus accumbens in rats.

The effects of dopamine-receptor antagonists on electrically-evoked dopamine release were compared in the nucleus accumbens and striatal slices of rats. (-)-Sulpiride induced a concentration-dependent increase in the evoked dopamine release from both regions, the increase in the nucleus accumbens being significantly greater than that in the striatum. Clozapine also increased evoked dopamine release from the nucleus accumbens, but not from the striatum. The haloperidol-induced increase in evoked dopamine release from the nucleus accumbens was less than that from the striatum. These findings indicate that, in terms of dopamine transmission, (-)-sulpiride and clozapine, but not haloperidol, predominantly affect the nucleus accumbens rather than the striatum. We have previously reported that the contribution of D3 receptors to the regulation of dopamine release from dopamine nerve terminals is much greater in the nucleus accumbens than that in the striatum. (-)-Sulpiride and clozapine have relatively higher affinity for D3 receptors than does haloperidol. The regional differences in responsiveness of dopamine release to dopamine antagonists could be due to the different affinities to D2 or D3 receptors of the dopamine antagonists.

Animals↗
PubMed1995

[Inhibitory effect of haloperidol on evoked dopamine release from striatal slices of the rat].

Haloperidol-induced changes in evoked dopamine (DA) release from striatal slices in rats were investigated. The dose-response curves for haloperidol to changes in the evoked DA release were found to be biphasic (small doses increased the release and large doses inhibited), which were shifted to the left by longer periods of superfusion with haloperidol. This rapid tolerance or inhibition of haloperidol-induced increases in evoked DA release was reduced or attenuated by the superfusion with acetylcholine (ACh) antagonists or B-HT920 and was enhanced by ACh agonists. The microinjection of kainic acid into the rat striatum 4 days before the experiment reduced the rapid tolerance or inhibition of the haloperidol-induced increase in evoked DA release. These data indicate that intrinsic ACh neurons in the striatum may play an important role in the induction of the rapid tolerance or inhibition of haloperidol-induced increase in evoked DA release from striatal slices in rats.

Acetylcholine↗
PubMed1995

Development of medullomyoblastoma from classical medulloblastoma following a long term latency.

A case of medullomyoblastoma is described. Partial removal of a cerebellar tumor was performed at the age of 21 months old, and histopathological diagnosis was medulloblastoma. Death occurred at 15 years of age, due to pneumonia and relapse of the tumor. Autopsy revealed well-differentiated muscular and ependymal components disseminated in the medulloblastic area. Immunohistochemically, desmin was positively detected in not only autopsy materials but also undifferentiated cells of the surgical specimens, suggesting prospective myoblastic differentiation.

Cerebellar Neoplasms↗
PubMed1994

Amantadine increases the extracellular dopamine levels in the striatum by re-uptake inhibition and by N-methyl-D-aspartate antagonism.

This study was performed to investigate the mechanism how amantadine increases the extracellular dopamine (DA) levels in the striatum in vivo. Local application of amantadine (1 mM, 40 min) to the striatum through the dialysis membrane significantly increased the extracellular DA levels. Coadministration of nomifensine (10 mM, 120 min), an inhibitor of neuronal DA uptake, into the perfusion fluid attenuated the amantadine-induced increase in DA outflow. The amantadine-induced increases in the extracellular DA levels were also inhibited by co-perfusion with Ringer containing high Mg2+ (15 mM, 120 min) or with MK-801 (1 microM, 80 min). These findings suggest that amantadine increases the extracellular DA levels in the striatum by inhibiting the re-uptake of DA and/or by blocking the channel in the N-methyl-D-aspartate (NMDA) receptor, which results in antagonism of NMDA receptor function.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1994

Differential effects of dopamine agonists on evoked dopamine release from slices of striatum and nucleus accumbens in rats.

The effects of dopamine receptor agonists on electrically evoked dopamine release from slices of nucleus accumbens were compared with the effects on release from striatal slices in rats. Apomorphine, which has equal potency at the dopamine D2 and D3 receptors, reduced the evoked dopamine release from both regions to the same extent (ED50, 0.42 microM for nucleus accumbens; ED50, 0.46 microM for striatum). Quinpirole or 7-[3H]hydroxy-N,N-di-n-propyl-2-aminotetralin (7-OHDPAT), which are much more potent at the D3 receptor than at the D2 receptor, reduced the evoked dopamine release from the nucleus accumbens (ED50, 0.12 microM for quinpirole; 0.02 microM for 7-OHDPAT) much more than the release from the striatum (ED50, 1.6 microM for quinpirole; 0.55 microM for 7-OHDPAT). These results suggest that the contribution of D3 receptors in nucleus accumbens to regulate dopamine release from dopamine nerve terminals is much greater than in striatum.

Animals↗
PubMed1994

Effects of N-ethylmaleimide on dopamine release in the rat striatum after repeated treatment with methamphetamine.

Effects of N-ethylmaleimide or forskolin on electrically evoked dopamine release were investigated in striatal slices of rats pretreated with methamphetamine. N-Ethylmaleimide and forskolin both enhanced the evoked dopamine release in a concentration-dependent manner. The enhancement by N-ethylmaleimide of spontaneous dopamine release was not abolished by tetrodotoxin; the electrically evoked release was abolished, irrespective of its magnitude. Moreover, N-ethylmaleimide prevented the inhibitory effect of the dopamine receptor agonist, 2-amino-6-allyl- 5,6,7,8-tetrahydro-4H-thiazolo(5,4-d)-azepine dihydrochloride (B-HT 920) and the stimulatory effect of the dopamine receptor antagonist, (-)-sulpiride, on the evoked dopamine release. In contrast, forskolin had no effect on the B-HT 920-induced inhibition and (-)-sulpiride-induced enhancement of the evoked dopamine release. These data indicate that release-modulating dopamine autoreceptors are N-ethylmaleimide-sensitive and forskolin-insensitive. As N-ethylmaleimide has been reported to inactivate Gi protein and to block the regulation of noradrenaline release by alpha 2-adrenoceptors, the present results suggest that N-ethylmaleimide inactivates inhibitory GTP binding proteins to block the regulation by dopamine autoreceptors of evoked dopamine release. Methamphetamine pretreatment, which caused behavioral sensitization to a challenge dose of methamphetamine, attenuated the stimulatory effect of N-ethylmaleimide but not forskolin on the evoked dopamine release. The data indicate that the repeated administration of methamphetamine reduces a function of N-ethylmaleimide sensitive signal transduction system, probably including inhibitory GTP binding protein.

Animals↗