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Biomedical subjects

R Oishi

Publications and source records attributed to R Oishi.

153 records · Page 9Linked to original sources
PubMed1978

Facilitation of muricide by dorsal norepinephrine bundle lesions in olfactory bulbectomized rats.

The role of the dorsal norepinephrine bundle in the occurrence of muricide was studied in olfactory bulbectomized rats. Although the incidence of muricide was 30% in the olfactory bulbectomized rat, it significantly increased up to 80% and 90% on the 5th and 10th day, respectively, after dorsal bundle lesion. Cortical norepinephrine content decreased by about 50% after dorsal bundle lesions. These results indicate that the dorsal bundle system plays an inhibitory role in the occurrence of muricide in olfactory bulbectomized rats.

Aggression↗
PubMed1977

Possible involvement of a central noradrenergic system in automutilation induced by clonidine in mice.

Automutilation induced by a single large dose of clonidine was potentiated by pretreatment with methamphetamine, caffeine and theophyline, while it was inhibited by acute administration of reserpine, alpha-methyl-p-tyrosine, phenoxybenzamine, phentolamine and chlorpromazine. L-Dopa, 5-hydroxytryptophan and p-chlorophenylalanine had no effect on this abnormal behavior. Biochemical studies on brain monoamines revealed that noradrenaline was markedly increased and dopamine slightly so, but 5-hydroxytryptamine was never changed by clonidine. These results suggest that a central noradrenergic system may be involved in automutilation induced by clonidine in mice.

5-Hydroxytryptophan↗
PubMed1975

Hyperdipsia induced by bilateral destruction of the locus coeruleus in rats.

Bilateral lesions in the locus coeruleus (LC) of rats induced a urinary disorder and hyperdipsia. Dilatation of the urinary bladder, urinary retention and hematuria with bleeding originating from the urinary bladder, occurred immediately after the lesioning and continued for 2-5 days. Water intake increased 4 days after the lesioning. This hyperdipsia persisted for at least 4 days and then gradually returned to the control level. Food intake decreased for the first 5 days, and then returned to the control level. Lesions in the ascending dorsal bundle (DB) originating from the LC also produced hyperdipsia, but not urinary disorder. Destruction of the ascending ventral vundle (VB) originating from the noradrenaline (NA) neurons in the medulla oblongata did not affect eating, drinking or urination. The LC- or DB-lesioning caused a significant reduction of NA in the whole forebrain except the hypothalamus, whereas VB-lesioning caused reduced NA in the hypothalamus. In LC-lesioned animals, no significant changes were observed in serum osmolarity, Na+, K+, albumin and glucose in serum, or in the excretion of urine in the water-loading test.

Animals↗
PubMed1975

Central cholinergic activation by chlorfenvinphos, and organophosphate, in the rat.

Effects of 2-chloro-1-(2, 4-dichlorophenyl) vinyl diethyl phosphate, chlorfenvinphos, on spontaneous EEG, EMG and ChE activity in the brain and red blood cells were investigated in male Wistar rats. Chlorfenvinphos up to 1 mg/kg p.o. did not affect the ChE activity and the awake-sleep cycle. In doses over over 2 mg/kg, the ChE activity in the brain and red blood cells significantly decreased. The spontaneous EEG showed a prominent arousal pattern and appearance of slow wave sleep and parasleep was markedly depressed. Maximum inhibition of brain ChE activity was obtained 3 hr after the treatment and lasted for more than 72 hr. The duration of arousal pattern was proportional to the doses, however, the awake-sleep cycle returned to control on the 2nd day and a rebound increase in parasleep occurred on the 3rd day. Atropine depressed the EEG arousal pattern induced by chlorfenvinphos, without affecting ChE activity in the brain. The brain noradrenaline level was not altered with chlorfenvinphos. These results indicate that the appearance of EEG arousal pattern after chlorfenvinphos may be derived from central cholinergic activation.

Animals↗
PubMedDate not supplied

Involvement of central histaminergic and cholinergic systems in the morphine-induced increase in blood-brain barrier permeability to sodium fluorescein in mice.

Morphine (5 mg/kg, s.c.) caused a submaximal increase in the brain level of sodium fluorescein administered i.v. Histamine H1-antagonists, diphenhydramine and mepyramine, given either i.p. or i.c.v., had no significant influence on the effect of morphine. H2-Antagonists, cimetidine and ranitidine, administered i.c.v., but not i.p., significantly inhibited the morphine effect. alpha-Fluoromethylhistidine, a specific histidine decarboxylase inhibitor (given i.p. and i.c.v.) and antimuscarinic drugs, atropine and biperiden, but not methylatropine (given i.p.) also significantly reduced the morphine effect. Physostigimine (i.p.) significantly enhanced the effects of 0.5 and 1 mg/kg of morphine. Similar effects of histaminergic and cholinergic drugs were also observed on the buprenorphine- and DAGO-induced increase in blood-brain barrier (BBB) permeability to sodium fluorescein. None of the treatments with 6-hydroxydopamine, alpha-methyltyrosine, 5,7-dihydroxytryptamine or p-chlorophenylamine had any significant effect on the morphine-induced increase in BBB permeability. These findings suggest that the activation of brain H2-receptors by neuronal histamine and muscarinic receptors by acetylcholine is involved in the increase in BBB permeability to sodium fluorescein caused by mu opioid receptor agonists.

Acetylcholine↗
PubMedDate not supplied

Effects of midbrain raphe stimulation and lesion on EEG activity in rats.

In order to clarify whether the dorsal raphe (d-R) and medial raphe nuclei (m-R) of the midbrain play a different role in EEG activity, the effects of either electrical stimulation or lesion of each raphe nucleus were examined in rats. After m-R stimulation, EEG activity changed to a marked drowsy pattern. D-R stimulation, however, failed to produce such effects. M-R lesion elicited a significant arousal in EEG. The change in hippocampal EEG was the most characteristic, i.e., synchronized waves with an extreme increase in voltage. D-R lesion did not produce such a change. The hippocampal EEG arousal was easily abolished by L-5-hydroxytryptophan without any change in the cortical EEG or behavior. These results suggest that the m-R plays a more important role than the d-R in regulating the hippocampal EEG activity, especially in inhibiting the appearance of high voltage synchronized waves in the hippocampus.

5-Hydroxytryptophan↗
PubMedDate not supplied

Pharmacological characterization of cyclosporine A-induced kaolin intake in rats.

Kaolin intake behavior of rats is known to be one of the useful animal models to evaluate the emetic and antiemetic actions of drugs. The present study was aimed at elucidating the pharmacological characterization of cyclosporine A (CsA)-induced kaolin intake in rats. Subchronic treatment (once a day for 3 days) with CsA produced a dose- and time-dependent increase in kaolin intake. Scopolamine (muscarinic antagonist), mepyramine (selective histamine H(1) antagonist) and diphenhydramine (H(1) and muscarinic antagonist) but neither domperidone (dopamine D(2) antagonist) nor ondansetron (serotonin 5-HT(3) antagonist) significantly inhibited CsA-induced kaolin intake. These findings suggest that an activation of central muscarinic and H(1) receptor is closely associated with CsA-induced kaolin intake in rats. Use of scopolamine and/or diphenhydramine may be possible regimens to alleviate and avoid nausea and vomiting in patients with CsA therapy.

Animals↗
PubMedDate not supplied

The evaluation of sizing accuracy of particle counters for parenteral drugs.

Our evaluation of electronic liquid-borne particle counter systems has shown that, for accurate measurement of particulate matter in injections, the half count values of voltage thresholds from the particle counter itself should be used in the calibration for the particle sizes being evaluated. The manual method which uses the half count values in the USP XXIII<788> was improved, and the validity of our calibration method was supported by the results based on the ratio test, at 10 microns to those obtained at 15 microns is between 1.5 and 3.5, as per the Seventh Supplement of USP XXII <788>. Additionally, computer-based systems with automated calibration routines which solve the approximate Gaussian distribution of calibration particles have advantages. For the proper determination of the sizing accuracy of a particle counter, criteria of the ratio test at 10 microns and 15 microns as per the Seventh Supplement of USP XXII <788> should be applied at all critical particle sizes.

Calibration↗