Biomedical subjects

H Yokoo

Publications and source records attributed to H Yokoo.

At least 91 records · Page 5Linked to original sources

PubMed1994

Effect of opioid peptides on dopamine release from nucleus accumbens after repeated treatment with methamphetamine.

The effect of opioid peptides on extracellular dopamine levels in the nucleus accumbens was compared between rats treated with methamphetamine and saline repeatedly (for 9 days) by using microdialysis. After the period of repeated treatment, the rats in both groups were kept for an additional 9 days without further treatment. Repeated administration of methamphetamine reduced the decreasing effect of dynorphin (10 microM), applied locally in the perfusate, and enhanced the increasing effect of [D-Ala2,MePhe4,Gly-ol5]enkephalin (DAGO, 10 microM) on the extracellular dopamine levels in the nucleus accumbens. It is possible that repeated treatment with methamphetamine leads to attenuation of the inhibition and enhancement of the stimulation of dopamine release from the nucleus accumbens via presynaptic dynorphin- and enkephalin-sensitive receptors, respectively.

Analgesics↗

PubMed1994

Opposite changes in the mesolimbic dopamine metabolism in the nerve terminal and cell body sites induced by locally infused baclofen in the rat.

Infusion of baclofen (10(-4) M, 1 h) into the ventral tegmental area (VTA), the cell body site of mesolimbic dopamine (DA) neuron system in conscious rats, caused a decrease in both axonal and somatodendritic DA release in this neuron system, when monitored by in vivo microdialysis using two probes simultaneously placed in both the NAC and the VTA. Levels of the metabolite of DA, 3,4-dihydroxyphenylacetic acid (DOPAC) in the VTA decreased significantly in a similar manner following infused baclofen into the VTA, however, a pronounced increase in DOPAC outflow was observed in dialysates from the NAC. This dissociated changes in DA metabolism observed in the NAC may possibly be derived from regulatory mechanisms via an autoreceptor located in the DA nerve terminals.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1994

Ligation-induced acute pancreatitis in rats and opossums: a comparative morphologic study of the early phase.

Bile and pancreatic duct ligation (BPDL) in rats does not induce severe acute pancreatitis but only mild inflammation, which is self-limiting and eventually leads to pancreatic atrophy. However, BPDL in opossums induces severe acute necrotizing pancreatitis which uniformly leads to death within 14 days. We compared pancreatic morphologic changes after 24 hr of BPDL in rats and opossums. Pancreatitis histology score and acinar cell ultrastructural changes were evaluated. In both species, BPDL was associated with significant increases in histology score compared to sham controls (5.0 +/- 0.3 vs 1.5 +/- 0.3 in rats, 5.3 +/- 0.4 vs 1.1 +/- 0.1 in opossums; mean +/- SEM, ANOVA, P < 0.05). However, there was no significant difference in histology score between rats and opossums following BPDL; histologic changes, such as white blood cell infiltration, acinar cell vacuolation, and focal acinar cell necrosis, were similar. Acinar cell ultrastructural changes after BPDL in both species included dilated endoplasmic reticulum and autophagic vacuole formation. These findings indicate that the early morphologic changes after BPDL in rats are quite similar to those seen early in the course of BPDL-induced acute necrotizing pancreatitis in opossums. As the rat is a more economical and convenient model to study than the opossum, this study supports the use of the rat model to conduct pilot studies of early events in the development of BPDL-induced acute pancreatitis. This study also suggests the potential for investigating mechanisms that may be present in the rat which protect against progressive and fatal acute necrotizing pancreatitis as observed in opossums after longer periods of BPDL.

Acute Disease↗

PubMed1994

A case of Pick's disease with unusual neuronal inclusions.

An autopsy case of unusual Pick's disease in a 61-year-old male is described. Findings included severe atrophy of the frontal and temporal lobes, pyramidal tracts and basal ganglia accompanied by numerous intraneuronal argyrophilic hyaline inclusions. His neurological symptoms were constantly progressive during the 12-year course, characterized by akinesia and emotional incontinence. The inclusions were round, well-demarcated, slightly eosinophilic and intensely argyrophilic bodies in the perikarya, and distributed mainly in the subiculum and Sommer's sector of the hippocampus, amygdala and affected gyri. Immunocytochemically, they contain antigenic determinants of both phosphorylated and nonphosphorylated neurofilaments, but were negative for ubiquitin. Ultrastructurally, they were composed primarily of skeins of neurofilaments intermingled with cell organelles. Tubular profiles studded with granular substances, previously reported as a feature of the generalized variant of Pick's disease, and Hirano body-like lattice structures were occasionally observed in the inclusions. This case represents a slowly progressive neurodegenerative disorder characterized by fronto-temporal lobar atrophy and might by categorized as a variant of Pick's disease. However, some unusual properties of neuronal inclusions may suggest a different pathogenesis from that in classical Pick's disease.

Dementia↗

PubMed1994

Differential changes in rat brain noradrenaline turnover produced by continuous and intermittent restraint stress.

This experiment was performed to investigate differential effects of continuous and intermittent restraint stress on noradrenaline (NA) turnover in brain regions of male Wistar rats by measuring levels of a major metabolite of NA, 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MHPG-SO4) levels, as well as by measuring levels of plasma corticosterone and organ weights of the thymus, spleen, and adrenal glands. Rats in the 15-min and 30-min intermittently stressed groups showed significantly larger increases in MHPG-SO4 levels in most brain regions relative to those in the 90-min and 180-min continuously stressed groups, even though the total stress duration was equal or shorter. Body weight loss and loss of relative thymus weight in the 15-min intermittently stressed groups were the most marked among the five treatment groups. These findings suggest that stress-rest cyclicity is critical in determining the extent of stress-induced brain NA turnover and peripheral physiological responses.

Animals↗

PubMed1994

[Effect of nitric oxide on central dopaminergic neurons].

Neuronal damage induced by ischemia involves various changes in neurotransmission. Nitric oxide (NO), a putative neurotransmitter and/or neuromodulator has some role in this neuronal damage. In the present study, the effect of NO on the terminal site of dopamine (DA) neurons in the rat striatum was examined using the microdialysis technique. First perfusion with sodium nitroprusside (SNP) as an NO donor increased extracellular DA (10 mM, 460%; 1 mM, 140%) in the striatum and decreased its metabolites. Pretreatment with tetrodotoxin (TTX, 5 microM), (+)-5-methyl-10,11-dihydro-5H-dibenzo [a,d] cyclohepten-5,10-imine hydrogen maleato (MK801, 1 microM) or muscimol (1 microM) inhibited SNP-induced increases in extracellular DA and decreases in DOPAC (TTX, complete block; MK801, 75% inhibition; muscimol, 80% inhibition). Second, extracellular NO, DA and DOPAC were measured in the gerbil striatum following 10 minutes of forebrain ischemia produced by occluding both carotid arteries. Occlusion of the carotid arteries also caused increases in extracellular NO and DA in the gerbil striatum (NO, 3000%; DA, 2800%). These findings suggest that NO-facilitated DA release occurs via interaction between glutamatergic and dopaminergic neurons. These changes are probably partially involved in the neurodegenerative phenomena following ischemia. It is also shown that simultaneous measurements of NO and DA using this technique may be useful in assessing ischemic changes in vivo.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1994

[Preemptive analgesia produced with epidural analgesia administered prior to surgery].

The effect of epidural analgesia administered before or during surgery on postoperative pain relief using continuous epidural infusion of the mixture of local anesthetics and narcotics was studied. Ninety patients undergoing abdominal hysterectomy were randomly allocated to three groups; thirty patients of group 1 who received general anesthesia alone, thirty patients of group 2 with epidural analgesia 20 min before the end of surgery under general anesthesia and thirty patients of group 3 with epidural analgesia plus general anesthesia before surgery. Epidural analgesia was induced with 2% mepivacaine solution 15 ml without epinephrine in group 2 and 3, and in group 3 followed with 5 ml of the same solution at one-hour intervals. General anesthesia was induced with thiamylal and maintained with nitrous oxide, oxygen and sevoflurane. Immediately after surgery, 5 ml of the mixture of 0.225% bupivacaine and 0.0005% fentanyl was injected epidurally and followed with continuous infusion of the same mixture at the rate of 2.1 ml.h-1 over 24 h. Visual analogue score and Prince-Henry score were significantly less in group 3 than in group 1 and group 2 at 4 hours and 24 hours after surgery (P < 0.01, P < 0.05 respectively). These results suggest that postoperative continuous epidural analgesia is more effective if the entrance of noxious stimuli into the central neural system is prevented by preincisional epidural block.

Analgesia, Epidural↗

PubMed1994

Small intestinal HIV-associated enteropathy: evidence for panintestinal enterocyte dysfunction.

To characterize the absorptive defect of AIDS enteropathy, we have used a D-xylose kinetic model of proximal absorption and correlated these findings with Schilling's test for cobalamin absorption, measurements of distal intestinal function. In addition, we compared findings between duodenal and jejunal biopsy and aspirations to determine whether additional information can be obtained by sampling the more distal site. Twelve consecutive patients with AIDS who had 3 to 14 loose bowel movements per day and two stool study results negative for pathogens, were admitted for study. D-xylose testing with oral and intravenous doses was used to determine the rate constants for D-xylose absorption, Ka, and the rate constant for nonabsorptive loss, Ko. Duodenal and distal duodenal-jejunal endoscopic aspirations and biopsies were also performed. Minimal histologic abnormalities were seen in either the proximal or distal biopsy sites. There were no significant differences in mucosal blunting, abnormalities of the enterocytes, lamina propria infiltrate, or presence of microorganisms between duodenal and distal duodenal-jejunal sites. Seventy-five percent had no identifiable pathogens. Ten of 12 patients had diminished Ka, elevated Ko, or both. Two patients had a normal Ka and Ko. Eight of 10 had an abnormal Schilling's test result. Percentage weight loss correlated negatively with Ka (r = 0.75; p = 0.013) and with Schilling's test results (r = 0.65; p = 0.043. Ka correlated positively with Schilling's test results (r = 0.82; p = 0.004).(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗

PubMed1993

Muscimol-induced increase in dopamine release and metabolism is not observed in kainic acid-lesioned striatum of conscious rats: an in vivo microdialysis study.

Local application of muscimol through the striatal dialysis membrane caused a significant increase in both dopamine release and dopamine metabolism in the striatum of conscious rats, however, both elevations induced by muscimol were significantly lower in the kainic acid-lesioned striatum when assessed with in vivo brain microdialysis. These findings show that intra-striatal muscimol indirectly stimulates nigrostriatal dopaminergic function by possibly causing an inhibition of striatal gamma-aminobutyric acid neurons.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1993

Psychological stress increases serotonin release in the rat amygdala and prefrontal cortex assessed by in vivo microdialysis.

The effects of psychological stress on serotonin (5-HT) release were studied in the basolateral amygdaloid nucleus and the prefrontal cortex in conscious rats with in vivo microdialysis. Psychological stress, wherein emotional factors were predominantly involved, significantly increased extracellular 5-HT levels in these two areas. These findings suggest that activation of serotonergic neurons in these brain regions is involved in the emotional and/or cognitive states in animals.

Acoustic Stimulation↗

PubMed1993

A CRF antagonist attenuates stress-induced increases in NA turnover in extended brain regions in rats.

We investigated the effects of intracerebroventricular (i.c.v.) administration of corticotropin-releasing factor (CRF) antagonist, alpha-helical CRF9-41 (ahCRF), on increases in noradrenaline (NA) turnover caused by immobilization stress in rat brain regions. Pretreatment with ahCRF (50 or 100 micrograms) significantly attenuated increases in levels of 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MHPG-SO4), the major metabolite of NA in rat brain, in the locus coeruleus (LC) region, and attenuated the MHPG-SO4/NA ratio after immobilization stress for 50 min in the cerebral cortex, hippocampus, amygdala, midbrain and hypothalamus. However, stress-induced increases in plasma corticosterone levels were not decreased significantly by pretreatment with ahCRF. These results suggest that CRF, released during stress, causes increases in NA release in extended brain regions of stressed rats.

Animals↗

PubMed1993

Facilitatory modulation of mesolimbic dopamine neuronal activity by a mu-opioid agonist and nicotine as examined with in vivo microdialysis.

Administration of either Tyr-D-Ala-Gly-MePhe-Gly(ol) (DAGO), a mu-opioid agonist, or nicotine into the VTA (A10) caused an increase in both dopamine (DA) and its metabolite levels in both the A10 region and DA nerve terminals in the nucleus accumbens of rats when assessed with dual probe brain dialysis. These findings show that DAGO and nicotine increase both axonal- and somatodendritic-DA release, as well as metabolic activity in mesolimbic DA neurons, possibly by inducing an increase in neuronal impulse flow.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1993

Dopamine formation from L-dopa administered exogenously is independent of dopaminergic neuronal activity: studies with in vivo microdialysis.

Extracellular dopamine (DA) levels in the steady state were not detected in the hippocampus of rats where sparse dopaminergic innervations were demonstrated. However, following L-DOPA (100 mg/kg i.p.) administration, extracellular DA was detected. Although tetrodotoxin (TTX, 1 microM) failed to prevent this phenomenon, the striatal DA peak disappeared with the addition of TTX (5 microM) into the perfusate and reappeared following L-DOPA (100 mg/kg i.p.) administration. These findings suggest that DA synthesis from L-DOPA, administered exogenously, is independent of the existence of dopaminergic neurons and that outflow of newly synthesized DA into the extracellular space is not coupled to neuronal activity.

Animals↗

PubMed1993

Chronic treatment with haloperidol modifies the sensitivity of autoreceptors that modulate dopamine release in rat striatum.

The effects of apomorphine or sulpiride on electrically evoked dopamine release from striatal slices of rats pretreated with haloperidol were investigated. Chronic haloperidol treatment (1 mg/kg per day for 21 days) significantly reduced electrically evoked dopamine release from striatal slices until 72 h after the last injection. The apomorphine-induced reduction and the sulpiride-induced increase in evoked dopamine release were significantly enhanced by the chronic treatment with haloperidol at 72 h after the last injection. The enhancement of the sulpiride-induced increase in evoked dopamine release was inversely correlated with the dopamine release evoked by the first stimulation in striatal slices from haloperidol-treated (r = -0.85, n = 12, P < 0.01) but not from saline-treated rats. These results suggest that an increase in the sensitivity of dopamine autoreceptors due to chronic treatment with haloperidol could partially account for the reduction in dopamine release from striatal slices of rats.

Animals↗

PubMed1993

Corticotropin-releasing factor enhances noradrenaline release in the rat hypothalamus assessed by intracerebral microdialysis.

Corticotropin-releasing factor (CRF) at a dose of 3 micrograms administered intracerebroventricularly (i.c.v.) elicited increases in noradrenaline (NA) release, which was assessed by intracerebral microdialysis in the anterior hypothalamus of conscious rats. These increases persisted until 140 min after infusion of CRF. These results indicate that CRF enhances NA release in the hypothalamus, an effect which may underlie the 'stress-like' properties of CRF.

Animals↗

PubMed1993

Corticotropin-releasing factor activates the noradrenergic neuron system in the rat brain.

The effect of corticotropin-releasing factor (CRF) on central noradrenaline (NA) metabolism was examined by measuring levels of the major metabolite of NA, 3-methoxy-4-hydroxy-phenylethyleneglycol sulfate (MHPG-SO4) in several rat brain regions. Various doses of CRF ranging from 0.5-10 micrograms injected ICV significantly increased MHPG-SO4 levels in several brain regions including the hypothalamus, amygdala, midbrain, locus coeruleus (LC) region, and pons + medulla oblongata excluding the LC region. Plasma corticosterone levels were also significantly increased after ICV CRF administration up to 0.5 micrograms. The present results that CRF not only elevates plasma corticosterone levels but also increases NA metabolism in many brain regions suggest its neurotransmitter and/or neuromodulator role exerting the excitatory action on central NA neurons.

Animals↗

PubMed1993

Focal enterocyte vacuolization. A new microscopic finding in the acquired immune deficiency wasting syndrome.

Vacuolization of duodenal enterocytes was found by light microscopic examination in five patients meeting the Centers for Disease Control criteria for the acquired immunodeficiency wasting syndrome. Four of these patients had chronic diarrhea and malabsorption as documented by an abnormal D-xylose test, whereas one patient had no diarrhea or malabsorption. Enterocyte vacuolization was patchy in distribution, although affected cells were most notable on villous tips. Staining with period acid-Schiff, acid-fast bacilli, periodic acid-Schiff following diastase treatment, Congo red, and alcian blue were negative, suggesting that vacuolization is due to lipid accumulation. Immunoperoxidase staining for the human immunodeficiency virus envelope protein gp41 was positive in lamina propria mononuclear cells in all five patients. The authors hypothesize that lipid accumulation represents an enterocyte response to injury, possibly by an indirect effect of the human immunodeficiency virus.

Adult↗

PubMed1993

Modulation of (-)-sulpiride-induced increase in electrically-evoked release of dopamine from rat striatal slices.

(-)-Sulpiride (10 nM-10 microM) in the superfusate, dose-dependently increased the electrically-evoked release of dopamine from rat striatal slices. (+)-Sulpiride had little effect on evoked release of dopamine up to 10 microM. Apomorphine inhibited electrically evoked release of dopamine, and this effect of apomorphine was antagonized by (-)-sulpiride. SCH23390 and forskolin had no effect on the (-)-sulpiride-induced increase in evoked release of dopamine. Treatment with the irreversible dopamine-receptor antagonist N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline caused a significant increase in evoked release of dopamine and prevented the (-)-sulpiride-induced increase in the evoked release of dopamine. These results indicate that the (-)-sulpiride-induced increase in evoked release of dopamine is due to antagonism of the activation of dopamine autoreceptors by endogenously released dopamine.

Adrenergic alpha-Antagonists↗