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  3. A thioacetamide-induced hepatic encephalopathy model in C57BL/6 mice: a behavioral and neurochemical study

A thioacetamide-induced hepatic encephalopathy model in C57BL/6 mice: a behavioral and neurochemical study

  • Arq Neuropsiquiatr. 2010 Aug;68(4):597-602. doi: 10.1590/s0004-282x2010000400022.
Aline Silva de Miranda 1,  David Henrique Rodrigues,  Luciene Bruno Vieira,  Cristiano Xavier Lima,  Milene Alvarenga Rachid,  Paula Vieira Teixeira Vidigal,  Marcus Vinicius Gomez,  Helton José Dos Reis,  Cristina Guatimosim,  Antônio Lúcio Teixeira
Affiliations

Affiliation

  • 1 Laboratory of Immunopharmacology, Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil.
PMID: 20730316 DOI: 10.1590/s0004-282x2010000400022
Abstract

Objective: Hepatic encephalopathy (HE) is a neuropsychiatric syndrome resulting from liver failure. In the present study, we aimed to standardize an animal model of HE induced by thioacetamide (TAA) in C57BL/6 mice evaluating behavioral symptoms in association with liver damage and alterations in neurotransmitter release.

Method: HE was induced by an intraperitoneal single dose of TAA (200 mg/kg, 600 mg/kg or 1,200 mg/kg). Behavioral symptoms were evaluated using the SHIRPA battery. Liver damage was confirmed by histopathological analysis. The glutamate release was measured using fluorimetric assay.

Results: The neuropsychiatric state, motor behavior and reflex and sensory functions were significantly altered in the group receiving 600 mg/kg of TAA. Biochemical analysis revealed an increase in the glutamate release in the cerebral cortex of HE mice.

Conclusion: HE induced by 600 mg/kg TAA injection in C57BL/6 mice seems to be a suitable model to investigate the pathogenesis and clinical disorders of HE.

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