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Biomedical subjects

K Mizoguchi

Publications and source records attributed to K Mizoguchi.

At least 55 records · Page 3Linked to original sources
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

Effects of a new platinum complex on male fertility in rats--collaborative work to determine the optimal period and optimal parameters to detect effects on male fertility in rats.

To assess the testicular toxicity induced by compound C, a new platinum complex being developed as an anti-cancer drug, the substance was intravenously administered to male rats at doses of 1, 3 and 10 mg/kg/day for 4 weeks and at doses of 0.3, 1 and 3 mg/kg/day for 9 weeks. Males were cohabited with non-treated females after these treatment periods and at sacrifice the genital organ weights and number of sperm in the testis were recorded and a histopathological examination performed. The females were sacrificed on day 13 of gestation and the numbers of corpora lutea, implantations and resorptions were counted. In the 4 weeks treatment 10 mg/kg/day group, the testis weight increased while the weights of the epididymides, seminal vesicles and prostate decreased significantly, and the number of sperm was significantly decreased. Extension of seminiferous tubules, vacuolization of spermatocytes, spermatids and Sertoli cells, and degeneration of spermatocytes and spermatids were observed by histopathological examination. Copulation and impregnation were not affected by treatment but the implantation rate was significantly decreased in the 10 mg/kg/day group. These results show that compound C has testicular toxicity like other platinum complexes and that organ weight, number of sperm, number of implantation and histopathological examination are useful for detection purposes. Treatment with compound C for 9 weeks did not affect male reproductive function in spite of severe general toxicity. This suggests that testicular toxicity should be detected after 4 weeks rather than 9 weeks treatment.

Animals↗
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

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

Phenotypic heterogeneity of an adult form of adrenoleukodystrophy in monozygotic twins.

We describe genetically proven monozygotic twins with the adult form of adrenoleukodystrophy with significant phenotypic heterogeneity. Myeloneuropathy was common to both patients, but cognitive impairment and affective symptoms with extensive demyelination in the brain were prominent in the older twin, while adrenal insufficiency was predominant in the younger twin. The younger twin, however, exhibited affective symptoms similar to those displayed by his elder twin 10 years later. These findings suggest that nongenetic factors are important in determining the phenotypic variation of adrenoleukodystrophy gene.

Adrenoleukodystrophy↗
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

Two species of antiganglioside antibodies in a patient with a pharyngeal-cervical-brachial variant of Guillain-Barré syndrome.

A patient with a pharyngeal-cervical-brachial variant of Guillain-Barré syndrome had anti-GT1a and anti-GD1a antibodies (IgG) in the serum. The activities of anti-GT1a antibodies were stronger than anti-GD1a antibodies and their activities declined later in the clinical course. These two different antibodies bound independently to each ganglioside in an absorption study with polystyrene beads coated with GT1a or GD1a.

Adult↗
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

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

Muscle cramp as the result of impaired GABA function--an electrophysiological and pharmacological observation.

We investigated the mechanism of cramps in 2 patients: a 48-year-old man with bulbospinal neuronopathy, and a 46-year-old man with amyotrophic lateral sclerosis. Cramps were quite easily induced by volitional exertion and high-frequency stimulation of the peripheral nerves. When an ulnar nerve was blocked with lidocaine at the elbow, no cramp was induced despite the application of high-frequency stimulation at the wrist. Diazepam (GABAA agonist) was effective in the first patient and baclofen (GABAB agonist) in the second, with no cramps induced in spite of increasing stimulation intensity. Impairment of interneurons mediated by GABA as the neurotransmitter is thought to be involved in the mechanism of the cramps.

Amyotrophic Lateral Sclerosis↗
PubMed1993

PAF-releasing factor in human serum and inflammatory exudate.

A factor responsible for releasing PAF produced in stimulated human polymorphonuclear leukocytes, which had been previously reported in human serum (Miwa et al. (1992) J. Immunol. 148, 872-880), was also confirmed to be present in inflammatory exudate. PAF-releasing factor, partially purified from human serum, was shown to possess higher affinity for PAF than for triacylglycerol, cholesterol ester, fatty acid or phosphatidylcholine. PAF bound to this factor aggregated washed rabbit platelets to the same extent as that bound to BSA, but was difficult to be hydrolyzed using PAF acetylhydrolase. These observations strongly suggest that PAF-releasing factor functions as a PAF carrier in blood and in the inflammatory response.

Carrier Proteins↗
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

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

Expression cloning of a sheep adreno-ferredoxin using the polymerase chain reaction.

In addition to the selective amplification of cDNA from total RNA by the PCR method, the distinctive properties of ferredoxin-expressing colonies can be used for cloning a ferredoxin cDNA. This strategy for cloning and expressing cDNA in E. coli was applied to a sheep adreno-ferredoxin. The expressed sheep ferredoxin showed a spectral pattern typical of [2Fe-2S] proteins. The amino acid sequence deduced from the DNA sequence showed that the mature form of sheep ferredoxin consists of 128 amino acid residues. This rapid and simple method for cloning and expressing cDNA can be applied to other ferredoxins.

Adrenal Cortex↗
PubMed1992

Stress induces neuronal death in the hippocampus of castrated rats.

Whereas loss of CA3 neurons in the hippocampus of monkeys which died of stress ulcers suggests that some structural changes may occur, there is no direct evidence that shows stress-induced irreversible changes of neurons. When rats were orchidectomized (castrated) and stressed by restraint and immersion in water for 15 min/day for 30 days, significant loss of hippocampal CA3 and CA4 neurons was observed. Furthermore, primary cultured hippocampal neurons survived shorter when treated with corticosterone. This neuronal loss was prevented by simultaneous administration of testosterone in vivo and in vitro. These findings indicate that stress can contribute to neuronal degeneration associated with hypogonadal conditions such as aging.

Androstanols↗