Biomedical subjects

R Oishi

Publications and source records attributed to R Oishi.

At least 127 records · Page 7Linked to original sources

PubMed1988

Involvement of Mu receptors in the opioid-induced increase in the turnover of mouse brain histamine.

The effects of i.c.v. injected selective ligands for mu and delta opioid receptors on histamine (HA) turnover in the mouse brain were investigated to determine the receptor subclasses involved in the neurochemical response to opioids. HA turnover was measured by the accumulation of tele-methylhistamine, a major metabolite of brain HA, after pargyline injection (65 mg/kg i.p.). The increase in the HA turnover induced by [D-Ala2,D-Leu5] enkephalin (0.5 microgram i.c.v.) was antagonized by naloxone (0.3 microgram i.c.v.) but not by ICI 174,864 (5 micrograms i.c.v.), a selective delta receptor antagonist. [D-Ala2,MePhe4,Gly(ol)5]enkephalin (DAGO; 0.1-0.5 microgram i.c.v.), a selective mu receptor agonist, produced an increase in the HA turnover, whereas [D-Thr2-Leu5]enkephalin, Thr (0.1-1.0 microgram i.c.v.), a selective delta receptor agonist, had little effect on the HA turnover. DAGO (0.1 microgram i.c.v.) also increased the steady-state level of tele-methylhistamine but not that of HA. The effect of DAGO was observed in various brain regions except for the hypothalamus, and it was the most marked in the striatum. DAGO (10(-7) and 10(-6) M) significantly increased the K+ (30 mM)-evoked HA release from mouse cerebral cortical slices without influencing on the spontaneous HA release. The enhancement of HA release induced by DAGO (10(-6) M) was blocked completely by naloxone (10(-6) M) but not by tetrodotoxin (10(-6) M). These results suggest that opioids with mu agonist activity increase brain HA turnover by facilitating HA release from nerve endings.

Animals↗

PubMed1987

Effects of pentagastrin and carbachol on the gastric histamine level in alpha-fluoromethylhistidine-treated mice and rats.

The gastric mucosal histamine level in mice increased by about 80% and 100% after fasting for 24 and 48 h, respectively. In non-fasted mice, alpha-fluoromethylhistidine (alpha-FMH), a specific histidine decarboxylase inhibitor, significantly decreased the histamine level, the reduction amounting to 35% and 49%, 2 h and 4 h after treatment, respectively. In mice fasted for 24 h, a significant decrease of 42% was observed 4 h after treatment. However, in mice fasted for 48 h, no significant decrease was seen even 4 h after alpha-FMH treatment. Therefore, the histamine-releasing effect of re-feeding and drugs on the gastric mucosa was examined in vivo, using animals fasted for 48 h and subsequently treated with alpha-FMH. Food given simultaneously with alpha-FMH to 48-h fasted mice significantly decreased the histamine level 4 h later. Pentagastrin and carbachol administered alone (0.25-2.0 mg/kg, i.p.) had no significant effect on the histamine level. However, the combined treatment with these drugs significantly decreased the histamine level. In rats fasted for 48 h and treated with alpha-FMH, pentagastrin (0.25 and 0.5 mg/kg, i.p.) but not carbachol (0.125-0.5 mg/kg, i.p.) caused a significant decrease in the mucosal histamine level. In contrast to mice, the effect of the combined treatment with pentagastrin and carbachol was not synergistic in rats. These findings suggest that gastrin acts synergistically with acetylcholine in the histamine release from the gastric mucosa in mice, whereas such synergism may not occur in rats.

Animals↗

PubMed1987

Effects of halothane, enflurane and pentobarbital on brain histamine dynamics in mice.

The effects of halothane, enflurane, ketamine and pentobarbital on brain histamine dynamics were examined in mice. Brain histamine and tele-methylhistamine, a predominant metabolite of brain histamine, were simultaneously measured by high-performance liquid chromatography with fluorescence detection. Anaesthesia with the four agents had no effect on brain histamine content. The tele-methylhistamine content significantly increased during 1 h and 2 h anaesthesia with halothane (0.051 mmol/l or 0.76 mol/l) and 2 h anaesthesia with enflurane (0.11 mol/l or 0.16 mol/l). Enflurane and pentobarbital significantly inhibited the histamine depletion induced by alpha-fluoromethylhistidine (50 mg/kg, intraperitoneally), a specific inhibitor of histidine decarboxylase, suggesting that these agents decrease the histamine turnover. However, halothane and ketamine were ineffective in this respect. These results emphasize that various anaesthetics have different influences on brain histamine dynamics. Since there have been findings suggesting that brain histaminergic systems are involved in physiological functions such as regulation of blood pressure, body temperature and hormone secretion, changes in the brain histamine turnover should be given due attention with regard to physiological changes during anaesthesia.

Anesthetics↗

PubMed1987

Involvement of opioid receptors in phencyclidine-induced enhancement of brain histamine turnover in mice.

When the histamine (HA) turnover in the brain of mice was estimated on the basis of the pargyline-induced accumulation of tele-methylhistamine (t-MH), a predominant metabolite of brain HA, the enhancing effect of phencyclidine (PCP) on the HA turnover was antagonized by a large dose of naloxone. However, a dopamine receptor antagonist haloperidol, which is also a potent sigma receptor antagonist, did not inhibit the effect of PCP on the HA turnover. [D-Ala2,D-Leu5]enkephalin, a prototypic delta opioid agonist, markedly enhanced the HA turnover. The effect of this peptide was demonstrated not only when the HA turnover was determined by the pargyline-induced t-MH accumulation but when it was estimated by the HA depletion induced by alpha-fluoromethylhistidine, a specific inhibitor of histidine decarboxylase. A sigma agonist, SKF-10047, and a kappa agonist, ethylketazocine, had no PCP-like enhancing effect on the HA turnover. These results suggest that PCP enhances the brain HA turnover in mice by stimulating, probably indirectly, endogenous opioid systems.

Analgesics, Opioid↗

PubMed1987

Noradrenergic involvement in catalepsy induced by delta 9-tetrahydrocannabinol.

In order to elucidate the role of the catecholaminergic system in the cataleptogenic effect of delta 9-tetrahydrocannabinol (THC), the effect of pretreatment with 6-hydroxydopamine (6-OHDA) or with desipramine and 6-OHDA and lesions of the locus coeruleus were investigated in rats. The cataleptogenic effect of THC was significantly reduced in rats treated with 6-OHDA and in rats with lesions of the locus coeruleus but not in rats treated with desipramine and 6-OHDA, as compared with control rats. On the contrary, the cataleptogenic effect of haloperidol was significantly reduced in rats treated with desipramine and 6-OHDA but not in rats treated with 6-OHDA or in rats with lesions of the locus coeruleus. These results indicate that noradrenergic neurons have an important role in the manifestation of catalepsy induced by THC, whereas dopaminergic neurons are important in catalepsy induced by haloperidol.

Animals↗

PubMed1987

Feeding-related circadian variation in tele-methylhistamine levels of mouse and rat brains.

Circadian changes in the brain histamine (HA) and tele-methylhistamine (t-MH) levels were studied in mice and rats after adaptation to an alternating 12-h light/dark cycle (lights on at 0600). Although there was no significant circadian fluctuation of the brain HA levels, the levels of t-MH, a major metabolite of brain HA, showed a marked circadian variation. In mice, the t-MH levels were about 80 ng/g from 1200 to 1800 but about two times higher values were obtained from 2400 to 0600 of the next morning. In rats, the t-MH levels ranged from 24 to 28 ng/g at 0600 and 1200, slightly increased at 1800, and reached at 2400 a peak twice as high as the levels seen during the light period. The t-MH levels again rapidly decreased during the subsequent 3 h. In mice fasted from 1200, the t-MH levels did not increase during the period of darkness. When mice were fed at 1200 after a 24-h fast, a significant increase in the t-MH levels was observed at 1800. There was no significant circadian variation of the HA and t-MH levels in the plasma of mice and rats. These results suggest that circadian variation in brain t-MH levels is related to feeding and possible subsequent changes in elimination of t-MH from the brain and/or turnover of HA in the brain. This phenomenon should be given due attention when HA dynamics in the brain are being assessed.

Animals↗

PubMed1987

Mechanism of the central hyperglycemic action of histamine in mice.

The effect of i.c.v. administration of histamine (HA) on the plasma glucose level was examined in mice. HA (0.09-180 nmol) increased dose-dependently the plasma glucose level, 30 min after the injection. Even a low dose of 0.45 nmol produced a significant effect. The pretreatment with metoprine, an inhibitor of HA-N-methyltransferase, heightened the peak of the hyperglycemic response markedly and prolonged the duration. Systemic administration of the H1-receptor antagonists mepyramine (0.5-2 mg/kg), chlorpheniramine (1-4 mg/kg) and promethazine (1-4 mg/kg), inhibited dose-dependently the HA-induced hyperglycemia, whereas an H2-receptor antagonist, cimetidine (80 nmol i.c.v.), was without effect. The hyperglycemic response to HA disappeared in bilaterally adrenalectomized mice. Although the treatment of mice with metyrapone reduced the plasma corticosterone level to less than 15% of the control value, the hyperglycemic response to HA was still observed. After the administration of HA, there was a significant elevation of plasma norepinephrine levels. Increase in the plasma epinephrine was more marked than the norepinephrine response. Pretreatment with phentolamine (5 mg/kg i.p.) but not propranolol (15 mg/kg i.p.) inhibited the HA-induced hyperglycemia by about 50% and the combination of same doses of phentolamine and propranolol blocked the response completely. These results suggest that the central hyperglycemic effect of HA is produced mainly by an increase in the sympathetic outflow, followed by an increase in catecholamine secretion from the adrenal medulla. It is likely that the stimulation of H1, but not H2, receptors in the brain is involved in this response.

Adrenalectomy↗

PubMed1986

Involvement of opioid and non-opioid mechanisms in footshock-induced enhancement of brain histamine turnover in mice.

Naloxone (1-10 mg/kg, i.p.) dose-dependently inhibited the footshock-induced elevation in levels of tele-methylhistamine (t-MH), a predominant metabolite of brain histamine (HA), although this compound had no effect on the HA dynamics in the non-shocked control mice. Footshock significantly enhanced the HA depletion induced by alpha-fluoromethylhistidine, a specific inhibitor of histidine decarboxylase. However, in mice treated with naloxone (5 mg/kg, i.p.) footshock did not significantly facilitate the alpha-fluoromethylhistidine-induced HA depletion. In mice which had been rendered morphine-tolerant following an s.c. implantation of a pellet containing 50 mg of morphine base 3 days before, footshock produced no significant elevation of the t-MH level. The treatment with alpha-methyl-p-tyrosine, p-chlorophenylalanine or atropine had no significant influence on the footshock-induced t-MH elevation. The t-MH elevation was the most marked in the midbrain. In the hypothalamus and pons-medulla oblongata, no significant change in the t-MH level was produced by footshock. These results suggest that footshock increases the HAergic activity in the mouse brain partly through activation of opioid-related mechanisms and that alterations in HA dynamics differ with region of the brain.

Animals↗

PubMed1986

Diazepam-induced decrease in histamine turnover in mouse brain.

The effect of diazepam on brain histamine turnover was examined in mice. The steady state levels of histamine and tele-methylhistamine remained unchanged following the i.p. administration of 0.2-20 mg/kg of diazepam. However, diazepam in doses over 5 mg/kg significantly decreased histamine turnover, as estimated from the accumulation of tele-methylhistamine after pargyline treatment. Other benzodiazepines such as chlordiazepoxide, nitrazepam and estazolam in high doses also decreased histamine turnover. The inhibitory effect of diazepam on histamine turnover was antagonized by the pretreatment with a benzodiazepine antagonist Ro 15-1788. The histamine turnover was significantly inhibited by 2 mg/kg of muscimol. Diazepam (0.2-1 mg/kg) markedly and dose-dependently potentiated the inhibitory effect of 1 mg/kg of muscimol from non-significant to highly significant levels. The potentiation by diazepam was also antagonized by Ro 15-1788. Therefore, diazepam probably decreases histamine turnover in the brain via the benzodiazepine-GABA receptor complex.

Animals↗

PubMed1986

Brain histamine turnover enhanced by footshock.

When footshock was given to mice at 15-s intervals for 30-120 min, there was a significant increase in the brain level of tele-methyl-histamine (t-MH), a predominant metabolite of brain histamine (HA). This footshock-induced elevation of the t-MH level also occurred in mice pretreated with pargyline but not in mice pretreated with metoprine. The footshock facilitated the HA depletion induced by a-fluoromethylhistidine. These results suggest that footshock increases the brain HA turnover.

Animals↗

PubMed1986

Comparison of effects of phencyclidine and methamphetamine on body temperature in mice: a possible role for histamine neurons in thermoregulation.

We compared the effects of phencyclidine (PCP) and methamphetamine on body temperature and brain histamine turnover in mice. Methamphetamine at 5 and 10 mg/kg produced dose-related increases in rectal temperature, whereas PCP given in the same doses had no significant effect. In mice pretreated with alpha-fluoromethylhistidine, an inhibitor of histidine decarboxylase, PCP produced a marked hyperthermia. PCP markedly accelerated brain histamine turnover, as measured by the accumulation of tele-methylhistamine, a predominant metabolite of brain histamine, following administration of pargyline. Methamphetamine had no significant effect on the histamine dynamics. These results suggest involvement of brain histaminergic neurons in the action of PCP but not methamphetamine, and the presence of a histaminergic thermoregulatory mechanism.

Animals↗

PubMed1986

Lack of evidence for the involvement of catecholaminergic mechanisms in the behavioral anti-methamphetamine effect of L-histidine in the mouse.

The effects of L-histidine (HIS) on the hypermotility and the changes in brain monoamine dynamics induced by methamphetamine (MAMP) were examined in mice. HIS (1000 mg/kg) completely inhibited the hypermotility induced by MAMP (1 mg/kg). MAMP (1 mg/kg) significantly increased the dopamine level and decreased the 3,4-dihydroxyphenylacetic acid level. MAMP (5 and 10 mg/kg) also produced changes in the levels of noradrenaline, serotonin and their metabolites. HIS administered alone caused no significant changes in the levels of these amines and metabolites, nor did it affect MAMP-induced alterations in monoamine dynamics. These results suggest that catecholaminergic mechanisms are not involved in the behavioral anti-MAMP action of HIS.

Animals↗

PubMed1986

Glucose modulates the release of histamine from the mouse hypothalamus in vitro.

The effect of glucose concentration on the in vitro release of histamine (HA) was examined, using two different preparations of the mouse hypothalamus. The HA and tele-methylhistamine released from whole blocks of the hypothalamus into the medium linearly increased during 2-h incubation in normal Krebs-Ringer bicarbonate solution in the absence of external depolarizing stimuli. The release of HA from this preparation depended on the temperature and Ca2+ in the medium and was progressively increased with decrease in the glucose concentration from 11.5 to 1 mM. The rate of the HA release was dependent on the absolute concentration of glucose and not on an abrupt change in the concentration. When slices of the hypothalamus were incubated in high K+ medium, a temperature- and Ca2+-dependent HA release was observed. At low concentrations of glucose, the K+ (20 mM)-induced HA release from the hypothalamic slices was also enhanced. Tetrodotoxin (10 microM) inhibited the enhancing effect of a low glucose concentration (2 mM) on the HA release by 60%, in both preparations of the hypothalamus. The possibility that the release of HA from the mouse hypothalamus is regulated by glucose concentration and that activation of neuronal Na+ channels is involved in the enhancement of the HA release by low glucose concentrations warrants further attention.

Animals↗

PubMed1986

Drug-induced changes in histamine and tele-methylhistamine levels in mouse peripheral tissues.

To clarify the histamine (HA) dynamics in peripheral tissues, effects of drugs on the tissue HA and tele-methylhistamine (t-MH) levels were studied in mice. alpha-Fluoromethylhistidine (50 mg/kg, i.p.) significantly decreased the HA level in the stomach, but not in the liver, heart, ileum, submandibular gland and skin of mice. This compound had no significant effect on the t-MH level in any tissue examined. In non-fasted and 24-hr fasted animals, the t-MH level in the liver, heart and ileum was significantly increased by treatment with aminoguanidine (10 mg/kg, i.p.) plus pargyline (65 mg/kg, i.p.). However, in mice fasted for 48 hr, this treatment was ineffective in increasing the t-MH level in the heart and ileum, suggesting that the t-MH level in some peripheral tissues is under the influence of the food intake. Even if HA is synthetized and then metabolized in the peripheral tissues, the size of the HA pool with a rapid turnover in each tissue except for the gastric tissue seems to be very small.

Animals↗

PubMed1986

Effects of GABA-mimetic drugs on turnover of histamine in the mouse brain.

The effect of GABA-mimetics on histaminergic activity in the mouse brain was investigated. Systemic administration of muscimol (2 and 5 mg/kg), THIP (5-15 mg/kg) and aminooxyacetic acid (AOAA) (25 mg/kg) but not baclofen (2.5-15 mg/kg) inhibited the pargyline (65 mg/kg)-induced accumulation of tele-methylhistamine (t-MH). There was no regional difference in the inhibitory effect of muscimol on the t-MH accumulation by pargyline treatment. Muscimol and AOAA also inhibited decrease in the histamine (HA) level induced by alpha-fluoromethylhistidine (50 mg/kg), a specific inhibitor of histidine decarboxylase. These results suggest that these GABA-mimetics reduce the HA turnover in the mouse brain.

Aminooxyacetic Acid↗

PubMed1985

Decrease in histamine turnover in the brain of spontaneously hypertensive rats.

Histamine (HA) turnover rate in the brain of spontaneously hypertensive rats (SHR) was determined by the accumulation of telemethylhistamine after pargyline treatment. The values in these SHR were lower than in the Wistar Kyoto rats, particularly in the hypothalamus and brainstem. However, chronic treatment with L-histidine had no effect on the development of hypertension in the SHR. The functional significance of the decreased HA turnover in SHR is discussed in relation to the pathogenesis of hypertension.

Age Factors↗

PubMed1985

Morphine-induced changes in histamine dynamics in mouse brain.

The effect of the acute morphine treatment on histamine (HA) pools in the brain and the spinal cord was examined in mice. Morphine (1-50 mg/kg, s.c.) administered alone caused no significant change in the steady-state levels of HA and its major metabolite, tele-methylhistamine (t-MH), in the brain. However, depending on the doses tested, morphine significantly enhanced the pargyline (65 mg/kg, i.p.)-induced accumulation of t-MH and this effect was antagonized by naloxone. A specific inhibitor of histidine decarboxylase, alpha-fluoromethylhistidine (alpha-FMH) (50 mg/kg, i.p.), decreased the brain HA level in consequence of the almost complete depletion of the HA pool with a rapid turnover. Morphine further decreased the brain HA level in alpha-FMH-pretreated mice. Morphine administered alone significantly reduced the HA level in the spinal cord, an area where the turnover of HA is very slow. These results suggest that the acute morphine treatment increases the turnover of neuronal HA via opioid receptors, and this opiate also releases HA from a slowly turning over pool(s).

Animals↗

PubMed1985

Changes in histamine metabolism in the mouse hypothalamus induced by acute administration of ethanol.

The effect of acute ethanol administration on histamine (HA) dynamics was examined in the mouse hypothalamus. The steady-state level of HA did not change after intraperitoneal administration of ethanol (0.5-5 g/kg), whereas the level of tele-methylhistamine (t-MH), a predominant metabolite of brain HA, increased when 3 and 5 g/kg of ethanol was given. Pargyline hydrochloride (80 mg/kg, i.p.) increased the level of t-MH by 72.2% 90 min after the treatment. Ethanol at any dose given did not significantly affect the t-MH level in the pargyline-pretreated mice. Decrease in the t-MH level induced by metoprine (10 mg/kg, i.p.), an inhibitor of HA-N-methyltransferase, was suppressed by ethanol (5 g/kg), thereby suggesting inhibition of the elimination of brain t-MH. Ethanol (5 g/kg) significantly delayed the depletion of HA induced by (S)-alpha-fluoromethylhistidine (50 mg/kg, i.v.), a specific inhibitor of histidine decarboxylase. Therefore, a large dose of ethanol apparently decreases HA turnover in the mouse hypothalamus.

Animals↗