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Biomedical subjects

R Oishi

Publications and source records attributed to R Oishi.

At least 145 records · Page 8Linked to original sources
PubMed1985

delta 9-Tetrahydrocannabinol decreases turnover of brain histamine.

Histamine (HA) is a neurotransmitter present in the brain. As there is little information on the effect of delta 9-tetrahydrocannabinol (delta 9-THC) on brain histaminergic activity, the possible delta 9-THC-induced changes in brain HA turnover were studied in rats and mice. Whereas various doses of delta 9-THC had no influence on the brain HA levels in these species, high doses of delta 9-THC reduced the content of tele-methylhistamine (t-MH), a predominant HA metabolite in the brain, in mice. A moderate dose of delta 9-THC was effective in decreasing the brain t-MH content in the rats. Pargyline (65 mg/kg i.p.) caused a 101 ng/g accumulation of t-MH in mice and an 80 ng/g accumulation of t-MH in rats 105 min after the injection. delta 9-THC significantly suppressed the pargyline-induced t-MH accumulation at 50 mg/kg in mice whereas only 2 mg/kg of this compound was effective in rats, when administered i.v. 15 min after pargyline treatment. delta 9-THC (50 mg/kg i.v.) delayed the depletion of neuronal HA in the mouse brain, as induced by treatment with a specific histidine decarboxylase inhibitor alpha-fluoromethylhistidine (50 mg/kg i.p.). delta 9-THC (30 and 100 microM) significantly inhibited the K+-induced release of endogenous HA from guinea-pig hypothalamic slices. These results suggest that delta 9-THC decreases HA turnover in the brain.

Animals↗
PubMed1985

Phencyclidine and the dynamics of mouse brain histamine.

The effects of phencyclidine (PCP) on the dynamics of brain histamine (HA) were examined in the mouse brain. PCP (2-10 mg/kg i.p.) dose-dependently elevated the level of tele-methylhistamine (t-MH), a predominant metabolite of brain HA, without altering the HA level. PCP also enhanced the accumulation of t-MH after administration of pargyline hydrochloride (80 mg/kg i.p.). PCP at 5 mg/kg facilitated the HA depletion produced by (S)-alpha-fluoromethylhistidine markedly (50 mg/kg i.v.), a specific inhibitor of histidine decarboxylase. Metoprine (10 mg/kg i.p.), an inhibitor of HA-N-methyltransferase, decreased the t-MH level and increased the HA level. In the metoprine-treated mice, PCP at 10 mg/kg had no significant effect on the t-MH level, whereas it significantly increased the HA level. The increase in the t-MH level after administration of PCP (5 mg/kg) was observed in various brain regions except the pons-medulla oblongata. These results suggest that, in mice, PCP increases the brain HA turn-over possibly by facilitating the release of HA.

Animals↗
PubMed1984

Neuronal histamine inhibits methamphetamine-induced locomotor hyperactivity in mice.

Whether central histaminergic (HAergic) neurons mediate the regulation of methamphetamine (MAMP)-induced hyperactivity was clarified. L-histidine (HIS; 500 and 1000 mg/kg i.p.) reduced the locomotor hyperactivity induced by MAMP (1 mg/kg i.p.) in mice, and the effect was significant only at 1000 mg/kg. HIS significantly elevated brain histamine (HA) levels, in both doses, whereas telemethylhistamine (t-MH) levels were elevated only at 1000 mg/kg. Pretreatment with alpha-fluoromethylhistidine, a histidine decarboxylase inhibitor, suppressed both behavioral and biochemical effects of HIS. Metoprine, a HA-N-methyltransferase inhibitor, increased brain HA levels, decreased t-MH levels and suppressed the MAMP-induced locomotor hyperactivity. It is concluded that central HAergic systems may play an inhibitory role on the MAMP-induced locomotor hyperactivity.

Animals↗
PubMed1984

Regional differences in the turnover of neuronal histamine in the rat brain.

The turnover rate of histamine (HA) and the half-life of neuronal HA were estimated in 9 regions of the rat brain following pargyline-induced accumulation of tele-methylhistamine (t-MH). The turnover rate was the highest in the hypothalamus (108.7 ng/g/hr). The striatum also showed a high turnover rate (80.2 ng/g/hr) despite much lower levels of HA and t-MH, as compared with the levels in the hypothalamus. The turnover rate was relatively high in the thalamus, cerebral cortex, amygdala and midbrain, but it was very low in the cerebellum. t-MH accumulation in the spinal cord was nil. The HA levels were reduced to various degrees (from nil to less than 40% of the control) by (S)-alpha-fluoromethylhistidine, depending on the regions studied. The neuronal HA content of each brain region was subsequently estimated, and the half-life of neuronal HA in each region was calculated. The half-life of neuronal HA was the shortest (7.7 min) in the striatum, while it was long (about 50 min) in the hypothalamus and thalamus. Half-life values of about 20 min were obtained in other regions. These results show the high levels of histaminergic activity in some parts of the telencephalon, thalamus and midbrain as well as the hypothalamus.

Animals↗
PubMed1984

Histamine turnover in the brain of different mammalian species: implications for neuronal histamine half-life.

The turnover of neuronal histamine (HA) in nine brain regions and the spinal cord of the guinea pig and the mouse was estimated and the values obtained were compared with data previously obtained in rats. The size of the neuronal HA pool was determined from the decrease in HA content, as induced by (S)-alpha-fluoro-methylhistidine (alpha-FMH), a suicide inhibitor of histidine decarboxylase. The ratios of neuronal HA to the total differed with the brain region. Pargyline hydrochloride increased the tele-methylhistamine (t-MH) levels linearly up to 2 h after administration in both the guinea pig and the mouse whole brain. Regional differences in the turnover rate of neuronal HA, calculated from the pargyline-induced accumulation of t-MH, as well as in the size of the neuronal HA pool, were more marked in the mouse than in the guinea pig brain. The hypothalamus showed the highest rate in both species. There was a good correlation between the steady-state t-MH levels and the turnover rate in different brain regions. Neither the elevation of the t-MH levels by pargyline nor the reduction of HA by alpha-FMH was observed in the spinal cord, thereby suggesting that the HA present in this region is of mast cell origin. The half-life of neuronal HA in different brain regions was in the range of 13-38 min for the mouse and 24-37 min for the guinea pig, except for HA from the guinea pig hypothalamus, which had an extraordinarily long value of 87 min. These results suggest that there are species differences in the function of the brain histaminergic system.

Animals↗
PubMed1983

Regional distribution of histamine and tele-methylhistamine in the rat, mouse and guinea-pig brain.

Regional histamine (HA) and tele-methylhistamine (t-MH) contents were determined in the rat, mouse and guinea-pig brain. The highest HA and t-MH levels were found in the hypothalamus of all species. Fairly high t-MH levels were observed in the amygdala of all species and in the guinea-pig hippocampus. The t-MH/HA ratio was higher in the regions of the telencephalon than in the diencephalon and brainstem. The cerebellum and spinal cord showed extremely low t-MH/HA ratios. These results suggest higher histaminergic neuronal activities in the hypothalamus and some regions of the telencephalon than in other parts of the brain.

Animals↗
PubMed1983

Determination of norepinephrine and its metabolites released from rat vas deferens using high-performance liquid chromatography with electrochemical detection.

We designed a rapid, simple and sensitive method for the determination of norepinephrine (NE) and its metabolites by reversed-phase high-performance liquid chromatography (HPLC) with electrochemical detection. NE, 3,4-dihydroxymandelic acid (DOMA), and 3,4-dihydroxyphenylglycol (DOPEG) were adsorbed on alumina and eluted with 0.2 N HCl. From the remaining solution, normetanephrine and 3-methoxy-4-hydroxyphenylglycol (MOPEG) were extracted with ethyl acetate in the presence of both borate buffer and K2HPO4. Vanillylmandelic acid was extracted with ethyl acetate after acidification of the solution with concentrated HCl. The combined ethyl acetate phase was evaporated and the residue was dissolved in 0.1 N HCl. A 50 mu1 aliquot of each eluate or solution was injected onto the HPLC. Detection limits ranged from 300 pg to 1 ng per initial sample. We used this method to determine substances in the medium following incubation of the rat vas deferens. Approximately 110 and 80 ng/g/10 min of DOPEG and MOPEG, respectively, were present under normal conditions. The electrical stimulation of tissues from the rat vas deferens led to increases in the levels of NE, DOPEG, DOMA and MOPEG. Normetanephrine and vanillylmandelic acid were not detected in the medium. This is probably the first documentation of the endogenous levels of NE and all its metabolites in medium containing tissue of the sympathetic nervous system.

Animals↗
PubMed1983

In vivo binding of naloxone to opioid receptors in morphine-dependent mice.

In vivo binding assay of opioid receptors for naloxone was tested in morphine-dependent mice. The content of naloxone in the brain (whole brain minus cerebellum) and cerebellum was determined as the total binding and non-specific binding, respectively, 20 min after the intravenous injection of [3H]-naloxone. Acute treatment with 8 mg/kg of morphine sulfate markedly enhanced the non-specific binding of naloxone. In contrast, withdrawal for 6 hr after 72 hr of implantation of morphine decreased the non-specific binding of naloxone. The Scatchard analysis of the specific binding revealed two binding sites. The apparent low affinity Kd values of both morphine-tolerant and morphine-withdrawn mice were significantly decreased when compared to their respective controls. The apparent high affinity Kd and the high and low Bmax values were not altered by the morphine dependent-tolerant state.

Animals↗
PubMed1982

Stereospecific accumulation of dihydromorphine and naltrexone by corpus striatal slices of morphine-dependent mice.

Stereospecific accumulation of [3H]dihydromorphine and [3H]naltrexone by striatal slices from morphine-dependent mice was examined in Krebs-Ringer bicarbonate medium. Striatal slices showed a saturable and stereospecific accumulation of both [3H]ligands. The accumulation constant of naltrexone, determined by Wilkinson's analysis, was significantly decreased in both morphine-dependent mice and dependent mice abruptly withdrawn for 6 hr. The maximal accumulation of naltrexone was not changed in withdrawn mice, but decreased in dependent mice. This could be due to the high concentration of residual morphine in the slices. There were no significant differences in the accumulation constant or maximal accumulation of dihydromorphine among the striatal slices from control, dependent and withdrawn mice. These data indicate that in morphine-dependent mice, there is an increased affinity of the opioid receptors for the narcotic antagonist, naltrexone but not for the agonist, dihydromorphine.

Animals↗
PubMed1982

The role of the locus coeruleus in regulation of seizure susceptibility in rats.

When studying the role of the locus coeruleus (LC) in the regulation of seizure susceptibility in rats, we found that bilateral LC lesion significantly lowered the electroshock seizure threshold for the tonic extension of forelegs. The pattern of maximal electroshock seizure was not affected by LC lesion, although the recovery time was slightly prolonged. In the pentylenetetrazol (PTZ) seizure threshold test, LC lesion significantly elevated the twitch threshold, but did not affect the threshold for the generalized clonic seizure or clonic convulsion. Incidence of the tonic extension in the PTZ seizure test tended toward an increase with LC lesion. Biochemical determinations revealed that LC lesion significantly decreased the norepinephrine contents in various brain regions as well as the 5-hydroxytryptamine contents of some brain regions, but not the 5-hydroxyindoleacetic acid contents. These results suggest that while the LC is involved in the regulation of seizure susceptibility, the involvement differs with various types of seizures.

Animals↗
PubMed1980

Effects of delta-9-tetrahydrocannabinol on the cardiovascular system, and pressor and behavioral responses to brain stimulation in rats.

Effects of delta-9-tetrahydrocannabinol (delta 9-THC) on the cardiovascular system, and pressor and behavioral responses to brain stimulation were investigated in rats. In urethane-anesthetized rats, intravenous administration of delta 9-THC (1, 2 and 5 mg/kg) produced a significant and transient dose-related rise but no fall in blood pressure. delta 9-THC at these doses also produced marked reduction in heart rate which was antagonized by atropine (0.5 mg/kg i.v.) or bilateral vagotomy. In freely moving rats with chronically implanted electrodes and arterial cannula implants, intraperitoneal administration of delta 9-THC (4, 6 and 8 mg/kg) induced a rise in blood pressure and marked bradycardia. Abnormal behavior such as catalepsy, walking backwards and pivoting was also observed. delta 9-THC failed to inhibit the pressor responses to electrical stimulation of the posterior hypothalamus and midbrain reticular formation, whereas the drug suppressed the behavioral responses to stimulation of both regions. It is concluded that the cardiovascular effects seen with delta 9-THC injection are mainly the result of alteration of the efferent vagal activity by acting on the central nervous system and a more potent influence is exerted on the behavioral changes than on autonomic responses to brain stimulation.

Anesthesia↗
PubMed1979

The role of locus coeruleus in decapitation convulsions of rats.

The role of the central norepinephrine (NE) system, especially the locus coeruleus (LC), in the occurrence of decapitation convulsions was investigated in rats. Intraspinal injection of 6-hydroxydopamine (6-OHDA) caused a significant inhibition of decapitation convulsions as shown by prolongation of the latency and shortening of the convulsion's duration, as well as decreasing the NE content of the spinal cord to 35% of the control value without affecting the NE content of the various regions in the brain. Chemical lesion of the descending bundle from the LC by treatment with 6-OHDA significantly inhibited decapitation convulsions in a similar manner. Moreover, there was a decrease in the NE content of the spinal cord and hypothalamus to 24% and 47% of the control value, respectively. Bilateral electrolytic lesion of the LC also significantly inhibited decapitation convulsions and decreased the NE content of the cortex and spinal cord to 15% and 74% of the control value, respectively. However, lesions of the dorsal and ventral NE bundle by treatment with 6-OHDA, which caused a marked decrease in the NE content of the cortex and hypothalamus, respectively, did not affect the decapitation convulsion. Intraspinal injection of 5,6-dihydroxytryptamine resulted in a decrease in the 5-hydroxytryptamine content of the spinal cord only; moreover, it did not change the decapitation convulsion. These results suggest that coeruleospinal NE neurons play an important role in the occurrence of decapitation convulsions.

5,6-Dihydroxytryptamine↗
PubMed1979

Possible involvement of brainstem norepinephrine in pentylenetetrazol convulsions in rats.

The thresholds of twitch and clonic convulsion induced by intravenous infusion of pentylenetetrazol (PTZ) were measured in rats treated with 6-hydroxydopamine (6-OHDA). In adult rats, intraventricularly applied 6-OHDA increased susceptibility to PTZ convulsions and decreased norepinephrine (NE) contents of the cortex, hypothalamus and brainstem. When 6-OHDA was applied intraventricularly at 8 days after birth, PTZ convulsion susceptibility was slightly decreased and brainstem NE content was significantly increased. However, the effects of 6-OHDA given at 20 days after birth were similar to those observed in adults. Significant decrease of cortical and hypothalamic NE contents, but no change in PTZ convulsion susceptibility, occurred following 6-OHDA injections into the dorsal and ventral NE bundles. These results suggest that the brainstem NE neurons play an inhibitory role on the development of PTZ convulsions.

Animals↗
PubMed1979

Effect of stimulation of locus coeruleus on the evoked potential in the amygdala in rats.

Effects of stimulation of the locus coeruleus (LC) on evoked potential in the medial amygdala elicited by stimulation of the olfactory bulb (OB-AME potentials) were studied in the gallamine-immobilized rats. The amplitude of the OB-AME potential was inhibited 27.5% by the conditioning stimulation of LC delivered 30 msec before the test stimulation. The inhibitory effect of LC was reduced by propranolol 5 mg/kg i.p., but not by phentolamine 10 mg/kg i.p.. This effect was also reduced by tetrabenazine 10 mg/kg i.p.. Methamphetamine 5 mg/kg i.p. produced considerable potentiation of the LC inhibitory effect and a reduction of the OB-AME potential itself. These results suggest that the LC plays an inhibitory role in the electrical activity of the medial amygdala.

Amygdala↗