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Hitoshi Miyaoka

Publications and source records attributed to Hitoshi Miyaoka.

27 records · Page 2Linked to original sources
PubMed2003

Nitric oxide induced heat shock protein 70 mRNA in rat hypothalamus during acute restraint stress under sucrose diet.

1. Sucrose feeding increases the level of stress-induced heat shock protein 70 mRNA in the rat hypothalamus. However, the mechanism by which a sucrose diet induces mRNA remains unclear. The issues investigated in this study were (1) whether a sucrose diet affects nitric oxide production in the hypothalamus, and (2) whether nitric oxide mediates the sucrose and stress-induced elevation of heat shock protein 70 mRNA. 2. To address the first question, we measured the level of nitrate, a final nitric-oxide-oxidation product measurable in vivo, using a microdialysis method. To address the second question, we administered a nitric oxide synthase inhibitor. NG-nitro-L-arginine methyl ester, prior to stress, then measured the mRNA level of heat shock protein 70 by the reverse transcription-competitive polymerase chain reaction method. 3. After the initiation of restraint stress, rats fed a sucrose-containing diet, unlike those fed standard chow, displayed a transient nitrate elevation. This nitrate elevation was attenuated by pretreatment with NG-nitro-L-arginine methyl ester. The mRNA level increases in rats fed a sucrose diet were dose-dependently attenuated by NG-nitro-L-arginine methyl ester. 4. These data suggest that a sucrose diet induces heat shock protein 70 under stress by enhancing nitric oxide production in the hypothalamus.

Animals↗
PubMed2003

Long-term imipramine treatment increases nitrate levels in the rat hypothalamus.

1. Animal experiments have shown nitric oxide synthase inhibitors to have antidepressant-like properties. However, the effects of clinically available antidepressants on nitric oxide production in the brain remain unclear. In the present study, we examined whether imipramine, a conventional antidepressant, changes the levels of type-II nitric oxide synthase mRNA and nitrate, a final nitric-oxide-oxidation product measurable in vivo, in the rat brain. 2. Type-II nitric oxide synthase mRNA was detected using a reverse transcription-polymerase chain reaction method and nitrate was measured with a combination of high-performance liquid chromatography and the Griess reaction. 3. In untreated rats, type-II nitric oxide synthase mRNA was not detected in the hypothalamus, hippocampus, cerebral cortex, brain stem, or cerebellum. However, after 28-day oral administration of imipramine, it was detected in every brain region tested. Nitrate levels in the hypothalamus and cerebral cortex increased after 28-day treatment. In the hypothalamus, nitrate levels increased dose-dependently. These dose-dependent nitrate level changes were prevented by pretreatment with a nitric oxide synthase inhibitor. Moreover, the preventive effect of NG-nitro-L-arginine methyl ester was reversed by coadministration of L-arginine, a nitric oxide substrate. 4. These results suggest that chronic imipramine treatment induces nitric oxide synthase gene expression in the brain, followed by augmented NO production.

Animals↗
PubMed2003

Plasma nitrate levels in deficit versus non-deficit forms of schizophrenia.

OBJECTIVE: To determine whether nitric oxide production levels differ in patients with deficit and non-deficit forms of schizophrenia. METHODS: We investigated plasma nitrate levels, an index of in vivo nitric oxide production, in patients with deficit syndrome (n = 11) and non-deficit syndrome (n = 14) and healthy controls (n = 12) with a combination of high-performance liquid chromatography and the Griess reaction. RESULTS: There was no difference found in mean plasma nitrite levels, but plasma nitrate levels of patients with deficit syndrome were significantly lower than those with non-deficit syndrome (28.0 [SEM 2.5] micromol/L v. 44.2 [SEM 5.5] micromol/L, p < 0.05). CONCLUSIONS: A decline in nitric oxide production may be involved in primary negative symptoms in schizophrenia.

Adult↗
PubMed2002

Antipsychotic, antidepressant, anxiolytic, and anticonvulsant drugs induce type II nitric oxide synthase mRNA in rat brain.

Nitric oxide synthase inhibitors have been regarded as potentially beneficial for psychiatric disorders such as depression and schizophrenia, though little is known about how nitric oxide synthases are affected by psychotropic drugs in the brain. Using reverse transcription-polymerase chain reaction analysis, we investigated the effects of short- and long-term oral treatments with several psychotropics on type II nitric oxide synthase gene expression in the rat brain. With maprotiline and fluvoxamine, enzyme mRNA levels were higher after a 28 day treatment than after 1 and 4 day treatments. Zonisamide, carbamazepine and diazepam also increased mRNA, though differences in levels between 1, 4 and 28 day treatments were not significant. These results suggest that psychotropics modulate the gene expression of type-II nitric oxide synthase in the brain.

Animals↗
PubMed2002

Enhancement of delayed release of dopamine in the amygdala induced by conditioned fear stress in methamphetamine-sensitized rats.

Behavior during conditioned fear stress, a form of psychological stress, and the release of dopamine in the amygdala were measured over time using methamphetamine-sensitized rats, which are considered to be a model of hypersensitivity and vulnerability to emotional stress associated with stimulant-induced psychosis and schizophrenia. Dopamine release in the amygdala showed a delayed increase following completion of freezing behavior induced by conditioned fear stress regardless of the presence or absence of methamphetamine-sensitization. Since methamphetamine treatment did not lower the basal level of dopamine in the amygdala, under the conditions of this study, methamphetamine was presumed not to show neurotoxicity. On the other hand, basal dopamine levels after 15 h of repeated electric foot shock were about 40% lower than those in the control group (p<0.0002). In addition, dopamine release following conditioned fear stress in animals repeatedly treated with methamphetamine increased significantly from 40 to 100 min after conditioned fear stress while the duration of freezing behavior or latency of the appearance of grooming were not different from those in the control group. The above results suggested that delayed dopamine release in the amygdala is a phenomenon strongly associated with the emotional context of conditioned fear stress, and hypersensitivity and vulnerability to stress are at least partially involved with the overreaction to stress.

Amygdala↗
PubMedDate not supplied

Acute stress disorder and posttraumatic stress disorder symptoms among patients severely injured in motor vehicle accidents in Japan.

OBJECTIVE: The prevalence of acute stress disorder (ASD) and posttraumatic stress disorder (PTSD) in seriously injured survivors of motor vehicle accidents (MVAs) in Japan was investigated. Furthermore, predictive factors in the early stage for development of PTSD were evaluated. METHOD: Subjects were consecutive samples (N=100) of patients hospitalized with severe MVA injuries surveyed at two time points: within 1 month after the MVA and then 6 months later. In the first survey, we conducted the Acute Stress Disorder Interview and compiled results of a self-rating questionnaire; in the second survey, we conducted a structured clinical interview via telephone. RESULTS: The prevalence of ASD and PTSD were 9.0% and 8.5%, respectively. The shift from ASD to PTSD was more pronounced when we included partial diagnoses of ASD and PTSD. Three predictive factors for PTSD were identified through multiple logistic analysis: ASD-positive, presence of persistent physical disability and physical injury severity. CONCLUSIONS: Even among severely injured MVA survivors, most acute stress symptoms subside over time. However, having ASD or partial ASD in the early stage, and the presence of physical disability as an aftereffect are strong predictive factors for PTSD. These findings validate the importance of evidence-based intervention for ASD to forestall PTSD.

Accidents, Traffic↗
PubMedDate not supplied

The amplification of somatic symptoms in upper respiratory tract infections.

To assess the cultural differences in the role of somatosensory amplification in Japan and North America, we re-examined the role of psychological amplification of objective physical symptoms, as measured by the Somatosensory Amplification Scale (SSAS), in 82 Japanese patients with upper-respiratory tract infections. Anxiety and depression were measured with the Hospital Anxiety and Depression Scale (HADS). We determined the association among continuous variables using the Spearman correlation coefficient. Next, we used multiple regression analysis and selected all symptoms as independent variables. The SSAS was significantly associated with all somatic symptoms. It was also closely related to discomfort, but the SSAS was not significantly correlated with either anxiety or depression. All somatic symptoms were not significantly correlated with the objective physical findings. Multiple regression analyses indicated that amplification by SSAS was a statistically significant predictor of the patient's somatic symptoms and discomfort. The objective findings did not significantly predict the patient's symptoms. Our study provides some empirical evidence regarding psychological amplification of objective physical symptoms, as measured by SSAS, in Japanese patients with upper-respiratory tract infections. Our findings suggest that there is no difference in the role of amplification of bodily sensations between Japanese and North Americans.

Adolescent↗