Search PubMed⌕ Search

Biomedical subjects

N Uchimura

Publications and source records attributed to N Uchimura.

At least 37 records · Page 2Linked to original sources
PubMed1998

Circadian rhythms of hormone concentrations in alcohol withdrawal.

We investigated the circadian rhythm of hormones (cortisol, melatonin) in alcoholic patients during and 1 month after alcohol withdrawal. Patients with delirium tremens had irregular serum hormone concentration rhythms during withdrawal, which normalized after the withdrawal period. Patients without delirium tremens had normal circadian rhythms even during the withdrawal period. We speculated that the disturbance of the biological oscillator, in terms of the decline of synchronizing function or the decrease in synchronizing factors, caused abnormal circadian rhythms of hormone release during delirium tremens.

Adult↗
PubMed1998

Time course of saliva and serum melatonin levels after ingestion of melatonin.

Salival and serum melatonin levels after melatonin ingestion were measured by gas chromatography-mass spectrometry. Ingestion of 3 mg melatonin caused a marked increase in serum melatonin (3561+/-1201 pg/mL) within 20 min, followed by a gradual decrease, but the level still remained higher than the basal level at 240 min after the ingestion. The saliva melatonin 60 min after the ingestion showed the highest level (1177+/-403 pg/mL) which was one-third of the plasma level. The saliva melatonin level was highly correlated with the serum level throughout the experimental period (r=0.82, P=0.0001). These data indicate that the measurement of saliva melatonin level may be a suitable indicator for the melatonin secretion into general circulation.

Adult↗
PubMed1997

Does plasma free-3-methoxy-4-hydroxyphenyl(ethylene)glycol increase in the delirious state? A comparison of the effects of mianserin and haloperidol on delirium.

Sixty-six patients (47 men, 19 women, mean age 65 years) with delirium were treated with mianserin (10-60 mg/day) or haloperidol (2-6 mg/day) at Kurume University Hospital. The clinical effects of these drugs were compared before and after treatment using the Delirium Rating Scale. At the same time, blood was sampled to analyse plasma mianserin, free-3-methoxy-4-hydroxyphenyl(ethylene)glycol (MHPG) and homovanillic acid concentrations. Marked improvement after 1 week was observed in 69.4% of patients undergoing mianserin treatment, and in 70.6% of those receiving haloperidol. A statistically significant difference in the clinical effects of these drugs was not observed. Although improvement in the delirious state and a decrease in the plasma free-MHPG concentration were observed after drug administration, the plasma free-homovanillic acid concentration showed no significant change. The higher plasma free-MHPG concentration in the delirious state suggests the existence of a preparatory state whereby noradrenaline metabolism is involved in the appearance of the abnormal behaviour associated with delirium. These data suggest that free-MHPG concentrations could potentially be used as a predictor of delirium.

Aged↗
PubMed1996

A patient with chronic hepatitis C and a history of abuse of analeptic drugs, who showed hallucination and delusion with interferon administration.

We experienced a case of chronic hepatitis type C accompanied with hallucination and delusion induced by interferon (IFN) therapy positive. The case was a 47-year-old male, whose laboratory data showed positive for anti-Hepatitis C Virus (HCV) and elevated transaminase level. He was treated with 6 MU/day of natural-type IFN-alpha (HLBI). Sleeplessness and delusions of persecution developed about 2 months after the start of IFN therapy. The interview of the psychiatrist disclosed that the patient had a history of addiction to drugs, and these psychiatric symptoms were diagnosed as being of "the flashback phenomenon." These side effects were improved after the administration of psychotropics and it was suggested that we had to take care of the development of flashback phenomenon during the treatment of IFN in cases of chronic hepatitis with a history of addiction to drugs.

Delusions↗
PubMed1995

Effects of hCRH on sleep and body temperature rhythms.

We investigated the effects of human corticotropin-releasing hormone (hCRH) on the sleep structure and body temperature rhythms of seven healthy young men. Polysomnographic recordings were obtained and body temperatures were monitored continuously for 48 h in each subject following the intravenous administration of saline or of 100 micrograms hCRH. The administration of hCRH was associated with a significant phase-advancement in body temperature rhythm vs the saline control. The administration of hCRH affected non-rapid eye movement (NREM) sleep by reducing significantly slow wave sleep (SWS) and sleep efficiency, whereas the percentage of sleep stages 1 and 2 were increased significantly. These changes in body temperature rhythms and sleep structure induced by hCRH resembled those observed in patients with endogenous depression, except for the findings during rapid eye movement (REM) sleep. We hypothesize that a hypersecretion of hCRH in patients with endogenous depression may help to explain the changes in body temperature rhythms and sleep structure often reported in such patients.

Adrenocorticotropic Hormone↗
PubMed1994

[Effects of mianserin hydrochloride on delirium: comparison with the effects of oxypertine and haloperidol].

Mianserin (10-60 mg), haloperidol (2-6 mg) and oxypertine (20-60 mg) were administered once before bedtime in patients with delirium in Kurume University Hospital. The therapeutic effects of these drugs were investigated in the pre- and post-treatment using Delirium Rating Scale (DRS: Trzepacz et al., 1988). Mianserin was observed to be effective on 67% of the cases, and haloperidol and oxypertine in about 60%. Based on the clinical results and on the measurement of plasma concentration of mianserin, mianserin was considered to be an effective drug particularly against delirium in elderly patients because the effect and plasma concentration of mianserin were observed in the early stage of treatment without any side effects. The reduction of plasma free-MHPG was accompanied with improvement in the delirious state. The reason for the changes in plasma free-HVA was unclear.

Adult↗
PubMed1993

Effects of zopiclone on slow wave sleep and spontaneous K-complexes for normal healthy young adults.

Benzodiazepine (BZD) hypnotics have been known to decrease, to some degree, human slow wave sleep (SWS) although they elevate the arousal threshold during sleep. Zopiclone (ZPC), a cyclopyrrolone hypnotic, has attracted the interest of sleep researchers because an increase in human SWS has been reported. Since the increase has not been fully confirmed by all of the studies, the authors investigated the effects of ZPC 10 mg on SWS and the K-complexes for 7 healthy young adults because there is evidence indicating that delta waves consisting of SWS and the spontaneous K-complexes are identical. SWS and st. 4 sleep did not decrease on any of the ZPC nights but st. 3 sleep showed a tendency to reduce on the 1st ZPC night. The frequency of the K-complexes decreased significantly on the 2nd ZPC night and tended to reduce on the 1st ZPC night. Moreover, a significant positive correlation was noted between the decrease rates of SWS and the K-complexes on both the ZPC nights. The authors, therefore, could not obtain any findings suggesting an increase in SWS with ZPC.

Administration, Oral↗
PubMed1992

A case of tardive Tourette-like syndrome.

We have had experience in treating tardive Tourette-like syndrome on a chronic schizophrenic patient. The patient was a 38-year-old woman. A diagnosis of schizophrenia was made in 1971 and she received repeated medications for 17 years. In 1989, she began to show vocal tic with coprolalia and motor tic. The medications were haloperidol 18 mg, zotepine 200 mg, levomepromazine 100 mg, biperiden 3 mg and nitrazepam 10 mg at the beginning of Tourette-like syndrome. We have tried to change the medications but this tardive Tourette-like syndrome continued to hang on. However, the symptoms gradually improved after a change in drugs; cessation of biperiden 3 mg and the administration of clonazepam 3 mg. The present case suggested that tardive Tourette-like syndrome might be a subtype of neuroleptic-associated tardive syndromes which might be treated with clonazepam.

Adult↗
PubMed1991

Distinct muscarinic receptors inhibit release of gamma-aminobutyric acid and excitatory amino acids in mammalian brain.

Intracellular recordings were made from neurons of rat lateral amygdala, nucleus accumbens, and striatum in vitro. Synaptic potentials mediated by gamma-aminobutyric acid and by excitatory amino acids were isolated pharmacologically by using receptor antagonists, and their amplitudes were used as a measure of transmitter release. Muscarine and acetylcholine inhibited the release of both gamma-aminobutyric acid and excitatory amino acids, but measurements of the dissociation equilibrium constants for the antagonists pirenzepine, 11-(2-[(diethylamino)methyl]-1-piperidinyl)acetyl-5,11-dihydro-6H-pyrido [2,3-b][1,4]benzodiazepine-6-one, methoctramine, and hexahydrosiladifenidol indicated clearly that different muscarinic receptors were involved (M1 and probably M3, respectively). The differential localization of distinct muscarinic receptor subtypes on terminals releasing the major inhibitory and excitatory transmitters of the brain could be exploited therapeutically in some movement disorders and Alzheimer disease.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1991

Baclofen and adenosine inhibit synaptic potentials mediated by gamma-aminobutyric acid and glutamate release in rat nucleus accumbens.

Intracellular recordings were made from rat nucleus accumbens neurons in a tissue slice in vitro; postsynaptic potentials (p.s.p.) were evoked by focal electrical stimulation of the slice surface. P.s.p. were partially blocked by bicuculline (30 microM), partially blocked by a combination of 6-cyano-2,3-dihydroxy-7-nitroquinoxaline (CNQX, 10 microM) and DL-2-amino-5-phosphonovaleric acid (APV, 30 microM) and completely blocked when all three antagonists were applied together. Both the gamma-aminobutyric acid (GABA)-mediated p.s.p. (in CNQX and APV) and the glutamate-mediated p.s.p. (in bicuculline) were inhibited by baclofen (10-300 microM), adenosine (10-300 microM) and N6-(2-phenylisopropyl)adenosine (0.1-3 microM). Theophylline competitively antagonized the action of adenosine with an apparent dissociation equilibrium constant of about 15 microM. Baclofen, adenosine and N6-(2-phenylisopropyl)adenosine caused small (less than 10 mV) hyperpolarizations; voltage clamp experiments indicated that this resulted from an outward potassium current. It is concluded that activation of GABAB receptors and adenosine A1 receptors inhibits the release of glutamate and GABA at synapses in the nucleus accumbens.

2-Amino-5-phosphonovalerate↗
PubMed1990

Actions of cocaine on rat nucleus accumbens neurones in vitro.

1. Intracellular recordings were made from 103 neurones of the rat nucleus accumbens in vitro. 2. Dopamine (3-100 microM; in sulpiride, 1 microM) hyperpolarized neurones (79%) by acting at D1 receptors: dopamine (3-100 microM; in SCH23390, 1 microM) depolarized neurones (55%) by acting at D2 receptors. 5-Hydroxytryptamine (1-100 microM) depolarized 86% neurones. 3. Both actions of dopamine as well as the effect of 5-hydroxytryptamine were potentiated by cocaine (0.3-30 microM), which had no effect of its own on membrane potential. 4. Dose-ratio was computed as [(concentration of agonist causing a 4 mV potential change in cocaine)/(concentration of agonist causing a 4 mV potential change without cocaine)]. Cocaine (1-30 microM) caused the same dose-ratio whether dopamine depolarizations (D2) or hyperpolarizations (D1) were measured; the dose-ratio ranged from 2 (1 microM) to 50 (30 microM). 5. Responses to 5-hydroxytryptamine were increased more than responses to dopamine; cocaine 1 microM gave a dose-ratio of 13.4 and at 30 microM gave a dose-ratio of 118. 6. It is concluded that cocaine acts to inhibit the uptake of dopamine and 5-hydroxytryptamine in slices of rat nucleus accumbens; lower concentrations of cocaine (0.3 to 1 microM) are particularly effective in potentiating the action of 5-hydroxytryptamine.

Animals↗
PubMed1990

Muscarine reduces inwardly rectifying potassium conductance in rat nucleus accumbens neurones.

1. Intracellular recordings were made from neurones in the nucleus accumbens in slices from the rat brain maintained in vitro. 2. Muscarine (1-100 microM) depolarized 101 of 107 neurones; this was associated with an increase in the input resistance. The potential change reversed polarity with conditioning hyperpolarization and the reversal potential was linearly related to the logarithm of the extracellular potassium concentration. 3. The depolarization caused by muscarine was not changed by tetrodotoxin (1 microM) or by a solution that contained lower levels of calcium (0.24 instead of 2.4 mM), higher levels of magnesium (5 instead of 1.2 mM) and cobalt (2 mM). 4. Muscarine caused an inward current and a decrease in slope conductance when applied to neurones voltage clamped near their resting potential (-82 mV). The current caused by muscarine reversed polarity at the potassium equilibrium potential. The current-voltage relation of the neurones between -60 and -120 mV was well fitted by assuming a voltage-independent potassium conductance and an inward rectifier potassium conductance; muscarine reduced predominantly the inward rectifier conductance. 5. Phorbol-12,13-diacetate (3 microM) and 5-hydroxytryptamine mimicked the action of muscarine. The inward currents caused by muscarine or 5-hydroxytryptamine were occluded by the inward current evoked by the phorbol ester. 6. The depolarization caused by muscarine was competitively antagonized by pirenzepine; the dissociation constant of 11 nM suggested involvement of the M1 receptor. 7. It is concluded that muscarine acts at M1 receptors to reduce the membrane potassium conductance and that activation of protein kinase C may be an intermediate step.

Action Potentials↗
PubMed1990

Cation current activated by hyperpolarization in a subset of rat nucleus accumbens neurons.

1. Intracellular recordings were made from neurons in slices of rat nucleus accumbens in vitro. Membrane currents were measured in the potential range -60 to -120 mV with the use of a single-electrode, voltage-clamp amplifier. 2. A minority of neurons (28/285) was identified that had resting membrane potentials almost 20 mV less negative than the majority of the cells. These cells, but not the majority, had an inward current that activated slowly when the cells were hyperpolarized from -60 to -120 mV. The time constant of activation was approximately 3 s at -70 mV and 100 ms at -120 mV. 3. This inward current was completely blocked by external cesium (2 mM) but unaffected by barium. The current was reduced in solutions containing low-sodium concentration and increased in solutions with high-potassium concentration; its reversal potential was estimated to be -36 mV. 4. It is concluded that two types of neuron can be distinguished in the rat nucleus accumbens on the basis of the presence or absence of a cation current activated by hyperpolarization. This current (IH, also called If and IQ) causes the neurons to have less-polarized resting potentials than the majority of nucleus accumbens neurons.

Animals↗
PubMed1989

Enhancement of dopamine actions on rat nucleus accumbens neurones in vitro after methamphetamine pre-treatment.

1. Intracellular recordings were made from the nucleus accumbens neurons in brain slices from rats previously treated with saline or methamphetamine. 2. In neurones from both methamphetamine- and saline (control)-treated rats, dopamine (0.1 mM) produced three types of responses: a biphasic response consisting of an initial hyperpolarization followed by a depolarization, a monophasic hyperpolarization and a simple depolarization. 3. Haloperidol (1 microM) reversibly suppressed both responses to dopamine; (-)-sulpiride (1 microM) selectively abolished the depolarization and prolonged the hyperpolarization. Forskolin (10 microM) and dibutyryl adenosine 3',5'-cyclic monophosphate (1 mM) mimicked the hyperpolarization. Both of the latter two substances were more effective in neurones from methamphetamine-treated rats than in neurones from control rats. 4. In slices from methamphetamine-treated rats, the dose-response curve for the dopamine hyperpolarization was shifted to the left of that seen in neurones from control rats by a factor of approximately 100. The dose-response curve for the dopamine depolarization was shifted to the right about 10-fold in neurones from rats treated with methamphetamine. 5. In slices from control rats, dopamine (less than or equal to 0.1 mM) and methamphetamine (less than or equal to 1 microM) had no effect on the EPSPs evoked by focal electrical stimulation of the periaccumbens regions: dopamine (greater than or equal to 10 nM) and methamphetamine (1 microM) markedly depressed the EPSPs in slices from methamphetamine-treated rats. Depolarizations evoked by application of exogenous glutamate were unaffected by dopamine (less than 5 microM). 6. In slices from methamphetamine-treated rats, dopamine (greater than or equal to 10 nM), forskolin (greater than or equal to 1 microM) and dibutyryl adenosine 3',5'-cyclic monophosphate (1 mM) depressed Ca2+-dependent spikes as well as the EPSPs. Haloperidol (1 microM) completely reversed the depressions of the EPSPs and Ca2+-dependent spikes by dopamine, while (-)-sulpiride (1 microM) was only partially effective. 7. These results indicate that chronic methamphetamine administration leads to enhancement of the actions of dopamine at D1 receptors located on glutamate and/or aspartate nerve terminals and of the dopamine hyperpolarization of principal neurones, which is also mediated by D1 receptors.

Action Potentials↗
PubMed1989

5-Hydroxytryptamine acts at 5-HT2 receptors to decrease potassium conductance in rat nucleus accumbens neurones.

1. Intracellular recordings were made from neurones in the nucleus accumbens in slices from the rat brain maintained in vitro. 2. 5-Hydroxytryptamine (5-HT.1-100 microM) depolarized 170 of 203 (84%) neurones and caused them to discharge action potentials. The depolarization was associated with an increase in the input resistance, and was reversed in polarity by conditioning hyperpolarization; this reversal potential was linearly related to the logarithm of the extracellular potassium concentration. 3. Application of 5-HT to neurones voltage-clamped near their resting potential (typically about -80 mV) caused an inward current and a decrease in the slope conductance. The current caused by 5-HT reversed polarity at the potassium equilibrium potential. Analysis with an equivalent circuit model of the neurone at steady state indicated that 5-HT selectively reduced the inward rectifier potassium conductance. 4. The depolarization caused by 5-HT persisted in tetrodotoxin (1 microM). It was reduced but not abolished by a solution that contained lower levels of calcium (0.24 instead of 2.4 mM), higher levels of magnesium (5 instead of 1.2 mM), and cobalt (2 mM). 5. The depolarization caused by 5-HT was competitively antagonized by the 5-HT2 antagonists ketanserin and mianserin with dissociation equilibrium constants of 3 and 45 nM respectively: spiperone (300 nM) also blocked the action of 5-HT. The depolarization was not mimicked or blocked by a number of other agonists and antagonists selective for the 5-HT1 and 5-HT3 receptor types.

Animals↗