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Effect of minaprine on "delayed neuronal death" in mongolian gerbils with occluded common carotid arteries.

Hiroaki Araki, +3 more
- 01 Aug 1987 - 
- Vol. 242, Iss: 2, pp 686-691
TLDR
Findings indicate that minaprine warrants further study for possible clinical prescription and that changes in the hippocampal neurons were exacerbated with time.
Abstract
The effect of the psychotropic drug minaprine on brain ischemia induced by a 5-min bilateral occlusion of the carotid arteries in the mongolian gerbil was studied. Severe impairment of memory was apparent when the passive avoidance test was carried out 2 days after the bilaterally induced ischemia. When minaprine in a dose of 50 mg/kg was given p.o. 30 min before the 5-min occlusion, there was a significant improvement in the memory impairment. The amplitude of the hippocampal theta waves decreased and Nissl's degradation was apparent in the CA1 neurons in the hippocampus from 2 days after the 5-min occlusion. Changes in the hippocampal neurons were exacerbated with time. When minaprine in a dose of 50 mg/kg was given there was no decrease in the amplitude of hippocampal theta waves, and Nissl's degradation and the destruction and disappearance of the CA1 neurons diminished considerably. All these findings indicate that minaprine warrants further study for possible clinical prescription.

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Riluzole, a novel antiglutamate, prevents memory loss and hippocampal neuronal damage in ischemic gerbils.

TL;DR: The neuroprotective effects of riluzole, a novel antiglutamate, has been demonstrated in a model of ischemia induced in female Mongolian gerbils by transient bilateral carotid occlusion and a clear-cut correlation was found between the deficit in the memory test and the decrease in muscarinic receptor binding in the CA1 fields.
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Neuroprotective actions of riluzole in rodent models of global and focal cerebral ischaemia

TL;DR: In focal ischaemia, provoked in Fischer rats following the occlusions of the middle cerebral artery, administration of riluzole (8 mg/kg) at 30 min and 24.5 h post occlusion significantly reduced the volume of infarcted cortex, which could be related to its inhibition of sodium channel activity, which in turn inhibits glutamate release.
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Ginseng root prevents learning disability and neuronal loss in gerbils with 5-minute forebrain ischemia

TL;DR: Findings suggest that RGP and CGS are effective in the prevention of delayed neuronal death, and that ginsenoside Rb1 is one of the neuroprotective molecules within ginseng root.
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Mechanism and pathogenesis of ischemia-induced neuronal damage

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