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Biomedical subjects

H Yokoo

Publications and source records attributed to H Yokoo.

At least 109 records · Page 6Linked to original sources
PubMed1993

Effects of benzamide derivatives on dopamine release from striatal slices of rats.

The effects of the benzamide derivatives, (-)-sulpiride, sultopride and nemonapride, on spontaneous and electrically evoked dopamine (DA) release from striatal slices of rats were investigated. Nemonapride at concentrations of 100 nM or higher caused a dose-dependent increase in spontaneous DA release from the slices. (-)-Sulpiride and sultopride had little effect on spontaneous DA release. The electrically evoked DA release was enhanced by (-)-sulpiride at concentrations of 100 nM or higher in the superfusate and reduced by nemonapride at 100 nM or higher. Sultopride caused a small increase in the evoked release of DA. The different activities of these drugs on DA release may account for the different clinical results they produce.

Amisulpride↗
PubMed1993

[The effect of CRF antagonist on immobilization stress-induced increases in noradrenaline release in rat brain regions].

We investigated the effects of intracerebroventricular (i.c.v.) administration of corticotropin-releasing factor (CRF) antagonist, alpha-helical CRF9-41 (ahCRF) on stress-induced increases in noradrenaline (NA) release in rat brain regions. Pretreatment with ahCRF (50 or 100 micrograms) attenuated significantly the stress-induced increases in levels of 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MHPG-SO4), the major metabolite of NA in rat brain, in the locus coeruleus region, cerebral cortex, hippocampus, amygdala and hypothalamus. Plasma corticosterone levels were not decreased significantly by administration of ahCRF. From these results, it is suggested that stress-induced increases in NA release in the rat brain regions are attenuated by ahCRF and thus that CRF, released during the stress, cause increases in NA release in these regions.

Animals↗
PubMed1992

L-threo-3,4-dihydroxyphenylserine, a noradrenaline precursor, inhibits dopamine release and metabolism in the rat striatum in vivo.

The effect of L-threo-3,4-dihydroxyphenylserine (L-threo-DOPS) on dopamine (DA) release and metabolism in the striatum was studied in freely moving rats by intracerebral microdialysis techniques. The DA level as well as the levels of 3,4-dihydroxyphenylacetic acid and homovanillic acid were significantly decreased 140 min after the administration of L-threo-DOPS (50 mg/kg intraperitoneally). The results suggest that L-threo-DOPS inhibits the release and metabolism of DA in the striatum.

Animals↗
PubMed1992

Attenuation of the inhibitory effect of dynorphin on dopamine release in the rat nucleus accumbens by repeated treatment with methamphetamine.

Dynorphin (1-100 nM) dose dependently inhibited both spontaneous and electrically evoked endogenous dopamine (DA) release from slices of the nucleus accumbens of untreated rats. When this inhibitory effect was compared, it was significantly reduced in rats pretreated (for 9 days) with methamphetamine (6 mg/kg per day i.p.) relative to rats treated with saline. These findings indicate that dynorphin inhibits DA release from the nucleus accumbens, and that treatment with methamphetamine reduces the modulatory action of dynorphin on DA release. It is possible that repeated administration of methamphetamine leads to attenuation of the inhibition of DA release from the nucleus accumbens via presynaptic dynorphin-sensitive receptors.

Animals↗
PubMed1992

Eating and drinking cause increased dopamine release in the nucleus accumbens and ventral tegmental area in the rat: measurement by in vivo microdialysis.

Dopamine (DA) release was simultaneously monitored in the nucleus accumbens (NAC) and ventral tegmental area (VTA) of conscious rats using in vivo microdialysis. During dialysis perfusion, rats were allowed access to food or water for 20 min following a 36 h food and water deprivation period. DA release increased significantly in the NAC and VTA in response to eating and drinking. The increases in both regions continued until 20-60 min after the end of the feeding or drinking session. These results show that the mesolimbic DA pathway is activated in response to ingestive behavior, and that DA release occurs in the cell body (A10) region as well as in the mesolimbic DA nerve terminals.

Animals↗
PubMed1992

Histopathologic findings of duodenal biopsy specimens in HIV-infected patients with and without diarrhea and malabsorption.

The significance of the human immunodeficiency virus (HIV) in the small intestinal lamina propria in patients with the acquired immune deficiency syndrome or conditions related to that syndrome who have chronic diarrhea and malabsorption is unclear. To investigate this issue, upper endoscopy (after a 12- to 16-hour fast) with duodenal biopsy and aspirate was performed in 20 HIV-infected seropositive homosexual men referred for diarrhea of more than 8 weeks duration (Group 2) and in 9 HIV-infected homosexual men referred for dysphagia or dyspepsia with no symptoms of malabsorption (Group 1). All biopsy specimens were examined by light microscopy and immunochemical staining with monoclonal antibody against HIV glycoprotein gp41. Electron microscopy was performed in 18 patients in Group 2 and in all patients in Group 1. Immunogold electron microscopy was used as a confirmatory test for identified HIV particles. In addition, D-xylose absorption was measured in all patients after a 25-g dose of D-xylose with measurement of serum D-xylose concentration 1 hour after the dose and measurement of 5-hour urinary D-xylose excretion. Mean serum D-xylose was 35.4 +/- 4.5 mg/dL in Group 1 and 15.8 +/- 2.3 mg/dL in Group 2 (P less than 0.001), whereas mean urine D-xylose was 5.5 +/- 0.6 g in Group 1 and 2.0 +/- 0.4 g in Group 2 (P less than 0.001). Immunoperoxidase for gp41 was positive in 5 (56%) patients in Group 1 and in 12 (60%) patients in Group 2. Lamina propria HIV viral particles were identified by electron microscopy in both patient groups. Viral particles were seen within and adjacent to the cytoplasm of mononuclear cells and were not present in enterocytes or neuroendocrine cells. There were no significant differences in serum or urine D-xylose tests between patients with and without lamina propria HIV. In addition, lipid accumulation in intercellular spaces near the basolateral membrane of adjacent enterocytes was seen in 33% of patients with chronic diarrhea. These findings suggest that lamina propria HIV is not a direct cause of enteropathy in HIV-infected patients and that lymphatic obstruction may be one pathophysiologic mechanism producing this malabsorptive state.

Biopsy↗
PubMed1992

Effects of angiotensin II on regional brain noradrenaline metabolism in non-stressed and stressed rats.

By measuring levels of noradrenaline (NA) and its major metabolite, 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MHPG-SO4), in various rat brain regions, the effects of angiotensin II (AT II) injected intracerebroventricularly (ICV) were investigated in non-stressed and stressed rats. Immobilization stress with a wire mesh was employed. Immobilization stress induced significant increases in MHPG-SO4 levels in all brain regions examined, i.e., hypothalamus, amygdala, thalamus, midbrain, hippocampus, cerebral cortex and locus coeruleus (LC) region, which suggests that stress increases NA release in these regions. AT II (1 and 10 micrograms), injected ICV 5 min before exposure to stress for 60 min, attenuated stress-induced increases in MHPG-SO4 levels in the hypothalamus, thalamus and amygdala. AT II, injected ICV in non-stressed rats at 65 min before sacrifice, significantly elevated MHPG-SO4 levels in the midbrain, cerebral cortex, thalamus and LC region. These results indicate that the attenuating effect of AT II on stress-induced increases in brain NA release are, in part, related to the reduction of fear and/or anxiety of the animals exposed to stress.

Angiotensin II↗
PubMed1992

[Regulation of (-)-sulpiride-induced increase in evoked dopamine release from striatal slices in rat].

The effects of dopamine (DA) agonist and antagonists on (-)-sulpiride-induced increase in electrically evoked DA release from striatal slices of rats were investigated. (-)-Sulpiride at concentrations of 10 nM to 1 microM in the superfusate caused a dose-dependent increase in electrically evoked DA release from the slices. (+)-Sulpiride had little effect on the evoked DA release up to 1 microM. Apomorphine inhibited the electrically evoked DA release which was antagonized by sulpiride. SCH 23390 and forskolin had no effect on the sulpiride-induced enhancement of evoked DA release. Pretreatment with the irreversible DA receptor antagonist, N-ethoxy-carbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ), caused a significant increase in evoked DA release and prevented the sulpiride-induced increase in evoked DA release. These results indicate that the sulpiride-induced increase in evoked DA release is due to an antagonism of the activation of DA autoreceptors by endogenously released DA.

Animals↗
PubMed1992

[der(1;7) (q10;p10) in three patients with malignant hematologic disorders].

The chromosome der(1;7) (q10;p10) is a derivative chromosome consisting of the short arm of chromosome 7 and the long arm of chromosome 1. We observed this abnormality in three patients with acute myeloblastic leukemia (AML), myelodysplastic syndrome (MDS), or myeloproliferative disorder (MPD). Case 1 was a 76-yr-old male with a history of IgG myeloma treated with melphalan, cyclophosphamide, vincristine, and prednisolone (MEVP). AML-M1 developed one and half years after discontinuation of the MEVP therapy. Case 2 was a 39-yr-old male with MDS. Case 3 was a 56-yr-old male with refractory anemia with excess of blasts in transformation that evolved from primary myelofibrosis. Chromosome analyses revealed der(1;7) (q10;p10) in bone marrow cells of the three patients. All patients failed to respond to chemotherapy, and died within four months after the diagnosis. Thus, der (1;7) (q10;p10) may indicate a very poor prognostic outcome in patients with malignant hematologic disorders.

Adult↗
PubMed1991

Changes in sensitivity of dopamine autoreceptors in rat striatum after subchronic treatment with methamphetamine.

To determine the functional alterations of the release modulating striatal dopamine (DA) autoreceptors that might be associated with the behavioral sensitization to methamphetamine after pretreatment with methamphetamine, we investigated the effect of apomorphine and sulpiride on electrically evoked DA release from striatal slices of rats pretreated with methamphetamine. Apomorphine induced a dose-dependent inhibition of the DA release evoked from the striatal slices. Pretreatment with methamphetamine (6 mg/kg per day for 9 days) significantly reduced the inhibitory effect of apomorphine. On the other hand, sulpiride caused a dose-dependent increase in the DA release evoked from the striatal slices. The enhancement by sulpiride of the evoked DA release was diminished by pretreatment with methamphetamine. These results show that pretreatment with methamphetamine blunts the responsiveness of evoked DA release to the DA antagonists as well as to the DA agonists, indicating that DA autoreceptor subsensitivity is produced by pretreatment with methamphetamine.

Animals↗
PubMed1991

Psychological stress increases dopamine turnover selectively in mesoprefrontal dopamine neurons of rats: reversal by diazepam.

The effects of psychological stress on catecholamine and indoleamine metabolism were examined in various brain regions of rats. Psychologically stressed rats were exposed to emotional responses of foot-shocked rats, but were themselves prevented from receiving foot-shock. Psychological stress for 30 min resulted in significant increases of both 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) levels in the medial prefrontal cortex (MPFC), but not in other dopamine (DA) terminal fields. The levels of noradrenaline (NA), serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) were unaffected in all brain regions examined after 30 min of psychological stress. A small but significant increase of DOPAC levels in the ventral tegmental area (VTA) was observed after a shorter (10 min) duration of stress. Moreover, an increase of DOPAC levels in the MPFC 30 min after psychological stress was attenuated by diazepam (5 mg/kg), and this attenuating effect was antagonized by Ro 15-1788 (15 mg/kg). These results suggest that mesoprefrontal DA neurons are selectively activated by psychological stress, and that the activation of the A10 cell body site (VTA) may precede that of the terminal field (MPFC). Moreover, diazepam was found to possess an inhibitory effect on the activation of mesoprefrontal DA neurons induced by psychological stress, and this effect may be partly mediated by benzodiazepine (BZD) receptors and implicated in the specific anxiolytic action of BZDs.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1991

Noradrenaline release in the rat amygdala is increased by stress: studies with intracerebral microdialysis.

The effects of immobilization and tail-pinch stress on extracellular noradrenaline (NA) release in the amygdala were studied in freely moving rats with intracerebral microdialysis techniques. After collection of basal levels of NA (2.63 +/- 0.26 pg/50 microliters/20 min), the rat was exposed to either immobilization stress or tail-pinch stress for 20 min. Immobilization and tail-pinch stress increased NA release to 250 and 243% of basal levels, respectively and the elevation of NA release was observed for 60 min and 40 min after release from stress, also respectively. These data suggest that microdialysis is a useful way to study extracellular NA release in the amygdala and that NA neurons in this region are activated by both immobilization and tail-pinch stress.

Amygdala↗
PubMed1991

Alterations in dopamine release from striatal slices of rats after chronic treatment with haloperidol.

The effects of chronic treatment with haloperidol on spontaneous and electrically evoked dopamine (DA) release from striatal slices of rats were investigated in vitro. DA was measured by high-performance liquid chromatography coupled to an electrochemical detector. The superfusion with haloperidol caused a dose-dependent (100 nM-100 microM) reduction in the electrically evoked DA release from striatal slices of rats, which was not antagonized by the superfusion with apomorphine. Chronic administration of haloperidol (1 mg/kg per day for 21 days) caused a significant reduction in electrically evoked DA release as well as in spontaneous DA release from striatal slices 24 h after the last injection. Moreover, pretreatment with haloperidol prevented the reduction of the DA release evoked in response to haloperidol superfusion (1 microM). These results indicated that chronic administration of haloperidol reduced DA release from striatal slices of rats, accompanied by tolerance for the inhibitory effect of drug superfusion on evoked DA release.

Animals↗
PubMed1991

Reconstituted basement membrane promotes morphological and functional differentiation of primary human prostatic epithelial cells.

Prostatic epithelial cells undergo rapid proliferation and lose their ability to synthesize and secrete prostate-specific antigen (PSA) and prostatic acid phosphatase (PAP) under standard tissue culture conditions. Herein, we compared the morphology, growth, secretory activity, and intermediate filament expression of human prostatic epithelial cells cultured on either standard tissue culture plastic or reconstituted basement membrane. Epithelial cells grown on plastic exhibited a 10-fold increase in proliferation and a higher percentage of cells in the S-phase of the cell cycle compared to cells cultured on basement membrane. However, cells grown on basement membrane secreted markedly higher levels of PSA and PAP. The basement membrane-induced enhancement of secretory activity was potentiated by dihydrotestosterone (DHT) and prostate stromal cell conditioned medium. Morphological studies showed that cells plated on basement membrane formed organoid-like clusters and maintained several aspects of differentiated epithelium including abundant secretory vesicles, microvilli, and desmosomes with associated cytoskeletal elements. Cultivation of epithelial cells on basement membrane components also suppressed the expression of vimentin, a mesenchymal intermediate filament polypeptide. However, cytokeratin expression was abnormal in cells grown on either surface. These results indicate that the differentiated properties of prostatic epithelial cells are promoted by cultivation on reconstituted basement membrane in the presence of DHT and stromal cell conditioned medium.

Acid Phosphatase↗
PubMed1991

Psychological stress-induced increases in noradrenaline release in rat brain regions are attenuated by diazepam, but not by morphine.

By measuring levels of noradrenaline (NA) and its major metabolite, 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MHPG-SO4) in the hypothalamus, amygdala and locus coeruleus region, we investigated the effects of diazepam 5.0 mg/kg, morphine 6.0 mg/kg, or naloxone at 5.0 or 10 mg/kg injected SC immediately before stress exposure, on increases in NA release caused by psychological stress. Psychological stress, wherein rats were exposed to emotional responses which were displayed by other electrically shocked rats, significantly increased MHPG-SO4 levels in the three brain regions examined and elevated plasma corticosterone levels. Both increases in brain MHPG-SO4 levels and elevations of plasma corticosterone levels induced by stress were attenuated significantly by diazepam but neither by morphine nor by naloxone. MHPG-SO4 levels in the hypothalamus and amygdala in the morphine-stress group were significantly higher than those in the saline-stress group. These findings suggest that psychological stress, in which an emotional factor is predominantly involved, causes increases in NA release in these brain regions examined and that these increases are attenuated only by diazepam, in contrast to the previous report, where increases in brain NA release caused by immobilization stress are attenuated not only by diazepam but also by morphine and are enhanced by naloxone.

Amygdala↗
PubMed1991

Kinetics of D-xylose absorption in patients with human immunodeficiency virus enteropathy.

D-Xylose absorption was studied in 12 patients with acquired immunodeficiency syndrome (AIDS) or advanced AIDS-related complex who had had diarrhea for more than 8 weeks, averaged an 11% (range, 3% to 21%) body weight loss during the previous 6 months, and had had negative stool examinations for enteric pathogens. Patients were evaluated by duodenal aspiration and biopsy and received both 25 gm oral and 10 gm intravenous doses of D-xylose. Kinetic analysis of D-xylose absorption was characterized by an absorption rate constant (ka) and a rate constant (ko) reflecting nonabsorptive loss. Extent of D-xylose absorption averaged 18.4% +/- 9.3% (+/- SD) in the 12 patients (normal greater than 60%). Percentage of weight loss during the previous 6 months was negatively correlated with ka (r = -0.69; p = 0.018) in the 11 patients in whom this parameter was reduced but was not correlated with either ko or extent of D-xylose absorption. In these patients with human immunodeficiency virus enteropathy, ka was reduced out of proportion to the minor histologic changes present in the duodenal biopsy specimens.

Acquired Immunodeficiency Syndrome↗
PubMed1991

Bile exclusion from the gut exacerbates acute pancreatitis caused by pancreatic duct obstruction in rats.

Acute pancreatic duct obstruction causes hyperamylasemia and mild pancreatic inflammation. We hypothesized that bile exclusion from the gut, which stimulates pancreatic secretion, exacerbates acute pancreatitis caused by pancreatic duct obstruction. Rats were surgically prepared with gastric, duodenal, bile, and pancreatic fistula catheters and a jugular vein catheter. After a 4-day recovery, groups of rats (a) served as controls, (b) had complete pancreatic duct obstruction for 6 h, or (c) had bile excluded from the gut for 24 h and then, during the final 6 h, complete pancreatic duct obstruction. Plasma amylase was measured, and all rats were euthanized at the end of experiments. Each pancreas was excised and weighed, and portions were fixed in formalin and glutaraldehyde. In blind fashion, each pancreas was examined under light microscopy and assigned a pancreatitis score based on presence of edema and severity of acinar cell changes and inflammation. Acute pancreatic duct obstruction was associated with increased pancreas weight, hyperamylasemia, and elevated pancreatitis score; moderate acinar cell vacuoles, which were observed in the cytoplasm near the basolateral membrane, and loss of microvilli were noted with electron microscopy. Bile exclusion from the gut exacerbated the acute pancreatitis caused by pancreatic duct obstruction; acinar cell distortion and destruction, as well as marked inflammation, were seen microscopically. These observations suggest that the absence of intestinal bile contributes to the pathogenesis of acute pancreatitis associated with pancreatic duct obstruction.

Acute Disease↗