Effect of minaprine on changes in monoamine contents in Mongolian gerbils with 5-min occlusion of common carotid arteries.

Araki, Hiroaki; Uchiyama-Tsuyuki, Yoshimi; Karasawa, Yasuko; Aihara, Hironaka

doi:10.1254/jjp.50.445

Cited by 7 publications

(6 citation statements)

References 19 publications

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“…Some of the present results are in accordance with those of the previous studies: for instance, increases in 3MT during ischemia (9) and increases in DOPAC and HVA after reperfusion (7, 9) have already been reported. It should be noted that the remarkably in creased levels of the substrates for MAO, 3MT and NM, during ischemia were rapidly elimi nated; and the metabolites by MAO, MHPG, DOPAC, HVA, and 5HIAA, accumulated shortly after reperfusion.…”

Section: Discussionsupporting

confidence: 94%

Participation of Type A Monoamine Oxidase in the Activated Deamination of Brain Monoamines Shortly after Reperfusion in Rats

Kumagae¹,

Matsui²,

Iwata³

1990

Japanese Journal of Pharmacology

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Abstract-Changes in monoamine levels during and after ischemia and effects of RS-8359, a type A monoamine oxidase (MAO-A) inhibitor, were studied in the cerebral cortex, hippocampus, and striatum of rats killed by microwave irradiation. The patterns of the changes in norepinephrine (NE), dopamine (DA), and serotonin (5HT) levels were similar during ischemia: All these monoamines decreased in all three regions. After reperfusion, however, the three monoamines showed different patterns of changes: NE, except in the striatum, decreased further; DA increased over the controls; 5HT remained suppressed in all three regions. With regard to the metabolites of the monoamines, the changes during and after reper fusion were almost similar in all regions: 0-methylated metabolites, normetanephrine and 3-methoxytyramine, markedly increased during ischemia; After reperfusion, the elevated levels of normetanephrine and 3-methoxytyramine returned to normal, while deaminated metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and 5 hydroxyindoleacetic acid, homovanillic acid (HVA), and 3-methoxy-4-hydroxy phenylethyleneglycol clearly increased. RS-8359 pretreatment (30 mg/kg, p.o.) at an hour prior to ischemia elevated the levels of NE in the cortex and hippocampus during ischemia and inhibited the increases in DOPAC and HVA levels and the decrease in 3MT levels at 30 min after reperfusion. These results suggest that deamination of NE, DA, and 5HT is activated by the increases in the substrates for MAO in all three regions, except the noradrenergic system in the striatum, and that MAO-A participates in the activated deamination after reperfusion.

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Section: Discussionsupporting

confidence: 94%

Participation of Type A Monoamine Oxidase in the Activated Deamination of Brain Monoamines Shortly after Reperfusion in Rats

Kumagae¹,

Matsui²,

Iwata³

1990

Japanese Journal of Pharmacology

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“…In addition, 2DG uptake of slices exposed to 20-min ische mia was impaired, and this impairment of 2DG uptake was also attenuated by the treatment with minaprine (10 and 100,uM). In the previous in vivo experiment, it was demonstrated that minaprine prevented both ischemia-induced hippocampal damage and the passive avoidance deficit (4,6). In addition, minaprine shows a protective effect against cerebral hypoxia and anoxia in a variety of animal models (15).…”

Section: Discussionmentioning

confidence: 97%

“…In addition, minaprine improves the memory impairment in Mongo lian gerbils (4) and in rats (5) caused by cerebral ische mia. Minaprine prevents both the reduction of hippo campal theta waves and a delayed neuronal death in the hippocampal CAI subregion induced by the bilat eral occlusion of the carotid arteries of Mongolian gerbils (6). In biochemical experiments, Muramatsu et al dem onstrated that minaprine increases the release of acetylcholine (ACh) from the hippocampus by a block ing action on the 5-HT2 receptors located on cholin ergic nerve terminals (7).…”

mentioning

confidence: 99%

Angiotensin II-Induced Pulmonary Edema in a Rabbit Model

Kodama

Shibata

Ueki

1997

Japanese Journal of Pharmacology

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ABSTRACT-Effect of minaprine on hypoxia or hypoxia/hypoglycemia (ischemia)-induced impair ment of 2-deoxyglucose (2DG) uptake by rat hippocampal slices was evaluated. Since minaprine was found to possess both a stimulating effect on acetylcholine release and a blocking effect on 5-HT2 re ceptors, the improving effect of minaprine on impaired 2DG uptake was compared to the findings obtained with oxotremorine, ketanserin and pentobarbital. Hippocampal slices were exposed to 20-min ischemia, and then these slices were returned to oxygenated and glucose-containing buffer for 6 hr. Ischemia reduced 30 mM KCI-induced 2DG uptake by the hippocampus. Pretreatment with minaprine, oxotremorine, pentobarbital and ketanserin attenuated the ischemia-induced decline of 2DG uptake. In addition, minaprine, oxotremorine and pentobarbital relatively recovered the increase of 2DG uptake in the hippocampal slices under hypoxia for 45 min. The present results suggest that minaprine exerts a neuroprotective action against ischemia-induced deficit of energy metabolism in vitro.

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“…We reported that in Mongolian gerbils with ischemia induced by 5-min bilateral occlusion of the carotid arteries, there was impairment of memory, abnormalities in the electroencephalogram and degradation of hippocampal CAI neurons (1,2). Various changes in monoamine contents caused by experimental ischemia have been documented (3)(4)(5) ; however, there were some differences in the reported data because the groups employed different species, ischemic periods and other conditions.…”

mentioning

confidence: 99%

Changes in monoamine contents in the brains of Mongolian gerbils following a 5-min occlusion of the bilateral carotid arteries.

et al. 1989

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Effect of minaprine on changes in monoamine contents in Mongolian gerbils with 5-min occlusion of common carotid arteries.

Cited by 7 publications

References 19 publications

Participation of Type A Monoamine Oxidase in the Activated Deamination of Brain Monoamines Shortly after Reperfusion in Rats

Participation of Type A Monoamine Oxidase in the Activated Deamination of Brain Monoamines Shortly after Reperfusion in Rats

Angiotensin II-Induced Pulmonary Edema in a Rabbit Model

Changes in monoamine contents in the brains of Mongolian gerbils following a 5-min occlusion of the bilateral carotid arteries.

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