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Biomedical subjects

M Fujiwara

Publications and source records attributed to M Fujiwara.

At least 793 records · Page 44Linked to original sources
PubMed1981

Pharmacological characteristics of abnormal behavior induced by harmine with special reference to tremor in mice.

Harmine, a hallucinogen with potent monoamine oxidase inhibitory properties, induced abnormal behavior, including tremor, scratching, head twitch and cage biting, in the mouse. A dose-dependent tremor was produced by all routes of administration of harmine. Although oxotremorine tremor was markedly suppressed by atropine, harmine tremor was unaffected by cholinergic drugs, remarkably inhibited by dopaminergic drugs, antidepressants and diazepam, mildly diminished by p-chlorophenylalanine, markedly augmented by 5-hydroxytryptophan and mildly increased by alpha-methyl-p-tyrosine. These findings suggest that a catecholaminergic (particularly dopaminergic) and serotonergic system imbalance plays an important role in the manifestation of harmine tremor. In view of these characteristics, harmine tremor may be useful as an effective experimental model for the evaluation of antiparkinsonism drugs, along with oxotremorine tremor because of the different mechanism of occurrence. In addition, harmine tremor appears to be useful in characterizing the properties of antidepressant drugs.

5-Hydroxytryptophan↗
PubMed1981

Effects of guanabenz on the adrenergic mechanism in rabbit arterial strips.

Effects of guanabenz, a hypotensive agent, on the adrenergic mechanism were studied in isolated rabbit thoracic aorta and pulmonary artery and findings were compared with data obtained with clonidine and guanethidine. Guanabenz in concentrations higher than 10(-6) M produced weak contractions which were attenuated by phentolamine or yohimbine. Such concentrations of guanabenz competitively inhibited the contractile response to noradrenaline, but did not attenuate the response to tyramine. In concentrations ranging from 10(-8) to 10(-7) M, guanabenz attenuated the contraction and the increase of 3H-efflux in response to transmural electrical stimulation of the pulmonary artery preincubated with 3H-noradrenaline. Phentolamine or yohimbine effectively blocked these inhibitory effects of guanabenz. Such effects of guanabenz were similar to those of clonidine and dissimilar to those of guanethidine. These results indicate that guanabenz acts on presynaptic and postsynaptic alpha receptors of the peripheral blood vessels, as in the case of clonidine and that the potency was almost the same as clonidine.

Animals↗
PubMed1981

Possible mechanisms of the triphasic effects of neurotensin on the rat blood pressure.

Neurotensin administered intravenously in a dose of 1 nmole/kg produced triphasic blood pressure responses in anesthetized rats: the first depressor, second pressor and third depressor responses. The first depressor response was significantly suppressed by treatment of animals with a mixture of diphenhydramine and metiamide or chronic administration of compound 48/80, but was not modified by treatment with atropine, phentolamine, yohimbine, propranolol, sulpiride and adrenalectomy. The second pressor response was abolished by phentolamine, yohimbine and adrenalectomy. The second phase response was also markedly reduced by diphenhydramine in reserpinized rats and chronic administration of compound 48/80. The third depressor response was blocked by treatment of animals with diphenhydramine or chronic administration of compound 48/80. These results suggest that neurotensin may produce an immediate depressor response (the first phase) partly through a histamine-mediated process, and the second pressor response is produced by catecholamines released from the adrenal medulla through a histamine-mediated process. The third depressor response appears to be mediated mainly by histamine. The participation of mast cells as an origin of histamine which mediates these processes is suggested.

Adrenalectomy↗
PubMed1981

Relationship between the effects of Goniopora toxin on action potential and on contractile force in guinea-pig papillary muscle.

Effects of Goniopora toxin (GPT) on cardiac action potential and on contractile force were investigated in isolated guinea-pig papillary muscle. GPT produced a positive inotropic effect by increasing contractile force and prolonging the relaxation time. The time-to-peak force was little affected. GPT prolonged the action potential duration but did not affect the resting membrane potential nor the amplitude of the action potential. Thus there was a correlation between the positive inotropic effect and prolongation of the action potential duration. Tetrodotoxin or a reduction in extracellular sodium concentration attenuated both the positive inotropic effect and the prolonged duration of the action potential induced by GPT. Lanthanum or a reduction in extracellular calcium concentration also inhibited the increased contraction but did not shorten the prolonged durations of contraction and action potential. Verapamil attenuated the positive inotropic effect by reducing both the contractile force and the duration of contraction, but did not shorten the action potential duration. These results show that the positive inotropic effect of GPT depends on the increase in both sodium and calcium influxes while the prolonging effect on the action potential probably depends only on an increase in sodium influx. Hence, it is concluded that the prolongation of the action potential due to the increased sodium permeability is an essential process for the appearance of the positive inotropic effect of GPT.

Action Potentials↗
PubMed1981

Noncholinergic, nonadrenergic contraction and substance P in rabbit iris sphincter muscle.

In the rabbit iris sphincter muscle, electrical transmural stimulation produced fast and slow components of contraction which were markedly attenuated by tetrodotoxin. The fast component was augmented by physostigmine and was abolished by atropine, while the slow component was little affected. Adrenergic and ganglionic blocking agents did not inhibit the slow component. Therefore, the fast component is probably cholinergic, while the slow one is noncholinergic, nonadrenergic in nature. Capsaicin did produce a considerable contractile response, but there was a gradual decline with repetitive application and a tachyphylaxis occurred. Under such conditions the slow but not the fast component was abolished. Substance P and acetylcholine produced the largest contraction, while ATP, histamine, serotonin and noradrenaline produced little or no response. In cold stored preparations, the responses to electrical transmural stimulation and capsaicin were either markedly attenuated or abolished, whereas substance P and acetylcholine produced considerable contractions. Baclofen and theophylline did not inhibit the slow response to electrical transmural stimulation or the response to substance P and capsaicin. Thus, electrical transmural stimulation produces cholinergic and noncholinergic, non-adrenergic contractions in the rabbit iris sphincter muscle and the latter response is considered to be mediated by substance P or a related peptide released from the neural component.

Acetylcholine↗
PubMed1981

Effects of CDP-choline on striatal dopamine level and behavior in rats.

To further assess the effects of CDP (cytidine diphosphate)-choline on Parkinsonian symptoms, striatal dopamine (DA) was measured fluorometrically in rats after injection of CDP-choline. CDP-choline (300 mg/kg, i.p.) increased the DA content in the striatum (p less than 0.05) one hour after injection. The behavioral effect of CDP-choline was then tested in rats in which the unilateral nigro-striatal DA neurons had degenerated following an intranigral injection of 6-hydroxydopamine (6-OHDA). CDP-choline alone did not produce behavioral changes in these rats. However, pretreatment with a single dose of CDP-choline (900 mg/kg, i.p.) suppressed both the apomorphine-induced contralateral and the d-amphetamine-induced ipsilateral circling. The same dose of CDP-choline suppressed the number of treadmill revolutions in mice. On the other hand, a 7-day consecutive treatment with 300 mg/kg of CDP-choline enhanced the apomorphine-induced contralateral circling (by 42%, p less than 0.05). The same treatment with CDP-choline raised the striatal DA content by 29% (p less than 0.05) on the intact side, but not on the 6-OHDA injected side. These results indicate that CDP-choline has either a direct nor an indirect DA agonistic effect. The increase in DA content, decrease in locomotion and enhancement of the effect of apomorphine can be explained on the hypothesis that CDP-choline may act as an antagonist on the DA neurons and receptors. The validity of this apparently paradoxical use of CDP-choline with antagonistic effect on DA neurons in the treatment of Parkinson's disease is discussed.

Animals↗
PubMed1981

Possible involvement of adenine nucleotides in sympathetic neuroeffector mechanisms of dog basilar artery.

The transmission mechanism of sympathetic neuroeffector was studied in the isolated dog basilar artery. Electrical transmural stimulation produced an initial contractile response which was followed by a transient relaxation or a late contraction, or both relaxation and contraction. These arteries showed a marked uptake of [3H]norepinephrine ([3H]NE) or [3H]adenosine after incubation with these compounds, and electrical stimulation increased the release of [3H]NE or 3H-purine compounds. After treatment with tetrodotoxin or bretylium or in the sympathetically denervated arteries, the mechanical response to electrical stimulation and the release of 3H-compounds were attenuated; however, the mechanical response was not affected by treatment with reserpine. These results suggest that transmural stimulation releases not only [3H]NE but also 3H-purine compounds predominantly from the sympathetic nerve terminals and produces sympathetic contractile and relaxing responses. Phentolamine enhanced these sympathetic responses and augmented the release of [3H]NE and 3H-purine compounds. Exogenously applied NE produced a slowly developing contractile response and inhibited the release of 3H-purine compounds upon electrical transmural stimulation. Exogenously applied ATP produced responses which were similar in pattern to the sympathetic response and the release of [3H]NE was inhibited. Other adenine nucleotides and adenosine produced only relaxation. Theophylline attenuated the relaxing response to sympathetic nerve stimulation or to exogenously applied nucleotides. These results suggest that ATP or related nucleotides are released, concomitant with NE, from the sympathetic nerve terminals in the dog basilar artery and may act as neurotransmitters and/or modulators on presynaptic and postsynaptic membranes.

Adenine Nucleotides↗
PubMed1981

Lipopolysaccharide-induced autoantibody response. II. Age-related change in plaque-forming cell response to bromelain-treated syngeneic erythrocytes.

In spleen of normal mice, there are relatively large numbers of plaque-forming cells (PFC) against syngeneic or allogeneic red blood cells treated with bromelain (Br. MRBC) and the numbers of PFC remarkably increase by the injection of bacterial lipopolysaccharide (LPS). In this report, age-related change in the anti-Br. MRBC PFC response was studied in vivo and in vitro. It was revealed that mean numbers of splenic anti-Br. MRBC PFC increased in both untreated and LPS-injected mice with age (3--14 months). The increase in anti-Br.MRBC PFC detected in LPS-stimulated spleen was dependent on the numbers of PFC in untreated spleen, but not related to the numbers of anti-TNP PFC nor the degree of 3H-thymidine incorporation assessed in in vitro culture. These results imply that enhanced anti-Br.MRBC PFC response was not merely due to polyclonal activation of B lymphocytes. Reasons for increased PFC numbers were analyzed in special references to suppressor activities. The experimental results were obtained suggesting that suppressors were not involved in anti-Br.MRBC PFC response. There were also no marked differences in the acceptability of suppressive signals between young and older spleen cells. It was concluded that hightened anti-Br.MRBC PFC response in older mice might be due to spontaneous increase in the size of Br.MRBC-reactive clone.

Aging↗