| DOI | Resolve DOI: https://doi.org/10.1016/S0028-3908(96)00158-X |
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| Author | Search for: Ligenhöhl, K.; Search for: Small, D. L.1; Search for: Monette, R.1; Search for: Buchan, A. M.; Search for: Morley, P.1; Search for: Allegrini, P. R.; Search for: Fröstl, W.; Search for: Sauer, D.; Search for: Schmutz, M.; Search for: Knöpfel, T. |
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| Affiliation | - National Research Council of Canada. NRC Institute for Biological Sciences
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| Format | Text, Article |
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| Abstract | We investigated the neuroprotective efficacy of the P-type Ca2+ channel antagonist daurisoline against electroshock-induced convulsions in rats and mice, hypoxic/hypoglycemic-induced damage in rat hippocampal slices and brain damage induced by occlusion of the middle cerebral artery (MCA) in rats. Daurisoline applied intravenously (i.v.) (bolus of 1–60 mg/kg) reduced the spontaneous activity of rat cerebellar Purkinje cells in a dose-dependent manner, a result demonstrating activity in the brain with systemic administration of the compound. While this effect reversed rapidly in about 10–20 min following bolus-application of the drug at doses of up to 30 mg/kg, a dose of 60 mg/kg consistently induced a depression of respiration followed by death of the animals. Daurisoline administered at 10–30 mg/kg did not prevent electroshock-induced convulsions in mice or rats, nor did it reduce neuronal damage in hippocampal slices induced by a hypoxic/hypoglycemic insult in vitro or by MCA occlusion in vivo. These observations do not support the hypothesis that P-type Ca2+ channels are promising drug targets for the acute treatment of epileptic convulsions and/or ischemic stroke. |
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| Publication date | 1997 |
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| In | |
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| Language | English |
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| NRC number | LIGENHOHL1997 |
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| NPARC number | 9363309 |
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| Export citation | Export as RIS |
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| Report a correction | Report a correction (opens in a new tab) |
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| Record identifier | cdcbb0c0-6270-48c4-93db-0b8851c811dd |
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| Record created | 2009-07-10 |
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| Record modified | 2020-03-20 |
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