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Effect of mannitol treatment on brain neurotransmitter markers in kainic acid-induced epilepsy
Authors:H Baran  H Lassmann  G Sperk  F Seitelberger  O Hornykiewicz
Affiliation:1. Department of Molecular Biosciences, School of Veterinary Medicine, University of California, Davis, 1089 Veterinary Medicine Drive, Davis, CA, 95616, USA;2. Department of Entomology and Nematology, and UCD Comprehensive Cancer Center, University of California, Davis, One Shields Avenue, Davis, CA 95616, USA;1. Department of Psychology, University of Illinois-Urbana Champaign, 603 E. Daniel Street, M/C 716, Champaign, IL 61820, USA;2. Neuroscience Program, University of Illinois-Urbana Champaign, 603 E. Daniel Street, M/C 716, Champaign, IL 61820, USA
Abstract:The effect of mannitol treatment on the behavioural, morphological and neurochemical brain damage induced after subcutaneously applied kainic acid (10 mg/kg) was studied in the rat. Mannitol at a dose of 1.5 g/kg was injected intravenously 10 min, 1.5 h and 3 h respectively after kainic acid administration. A protective effect of mannitol was observed only when mannitol was given 1.5 h after kainic acid application, i.e. within the early phase of kainic acid-induced brain oedema development. At this time period, mannitol prevented the development of kainic acid-induced seizures as well as irreversible brain lesions and neurochemical changes, the latter being reduction of noradrenaline levels in amygdala/pyriform cortex measured 3 h, and reduction of glutamate decarboxylase and choline acetyltransferase activities measured 3 days after kainic acid treatment. Similarly loss of glutamate decarboxylase activity in dorsal hippocampus induced by kainic acid was prevented by mannitol treatment. It is concluded that by washing out brain oedema, mannitol treatment may prevent propagation of seizures and brain damage in the kainic acid model of epilepsy.
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