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Chronically administered 3-nitropropionic acid induces striatal lesions attributed to dysfunction of the blood-brain barrier.

H Nishino·Y Shimano·M Kumazaki·T Sakurai
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Abstract

3-Nitropropionic acid (3-NPA), an irreversible inhibitor of succinate dehydrogenase, was administered to rats and the characteristics of the neuronal damage were investigated. Injections of 3-NPA (15 mg/kg s.c.) every 2 or 3 days for 1-2 weeks induced a mild neuronal loss and neutrophil invasions in the striatum (STR). The same administration for 4 weeks induced specific symmetric lesions in the lateral STR although the size was variable in each animal. Inside the lesions, strong neutrophil invasions and a strong immunoreaction for IgG, C3 as well as complement factor C3b/C4b receptor (C3b/C4br) were detected. Lesioned sites lost the immunoreaction for GFAP while the marginal areas contained abundant GFAP-labeled astrocytes around the vessels. In intoxicated animals, there was a weak but stout immunoreaction for IgG and C3b/C4br localizing around vessels in the STR even when there were no lesions or neuronal loss. The data suggest that the blood-brain barrier dysfunction is responsible for the specific vulnerability of the STR for the toxin.

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AnimalsAntihypertensive AgentsBlood-Brain BarrierBrain DiseasesComplement C3bComplement C4bGlial Fibrillary Acidic ProteinImmunoglobulin GImmunohistochemistryMaleNeostriatumNerve DegenerationNitro CompoundsPropionatesRatsRats, WistarJournal ArticleResearch Support, Non-U.S. Gov't

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H Nishino, Y Shimano, M Kumazaki, T Sakurai. 1995-02-17. Chronically administered 3-nitropropionic acid induces striatal lesions attributed to dysfunction of the blood-brain barrier.. https://doi.org/10.1016/0304-3940(95)11311-j

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