[HTML][HTML] A thioacetamide-induced hepatic encephalopathy model in C57BL/6 mice: a behavioral and neurochemical study
AS Miranda, DH Rodrigues, LB Vieira… - Arquivos de neuro …, 2010 - SciELO Brasil
Arquivos de neuro-psiquiatria, 2010•SciELO Brasil
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 …
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 …
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 600mg/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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