Introduction: In chronic liver failure, detoxification processes are impaired and resulting hyperammonemia leads to hepatic encephalopathy. In this disease, neurotransmitter systems are affected leading to cognitive and motor disorders. Protein kinase C gamma (PKCγ) as a key molecule in the signaling pathways of neurotransmitter receptors plays a main role in the processing of cognitive and motor functions. It is possible that PKCγ to be affected in hepatic encephalopathy. Therefore, the aim of the present study was to investigate gene expression of protein kinase C gamma in the prefrontal cortex, cerebellar cortex and hippocampus of rats with hepatic encephalopathy. Methods: Male Wistar rats weighing 300-350 g were used. For induction of hepatic encephalopathy a common bile duct ligation and transection was made but sham control operation consisted of laparotomy and bile duct identification without ligation and resection. On day 28 after the surgery, the animals were decapitated and their brain areas including the prefrontal cortex, the cerebellar cortex and the hippocampus were bilaterally dissected from cerebral hemispheres. A semi-quantitative RT-PCR method was used for evaluating gene expression of the PKCγ in the mentioned brain areas. The results of gene expression between the sham control group and the group with hepatic encephalopathy were analyzed with independent t-test. Statistical significant level was defined as P<0.05. Results: The results of the protein kinase C gamma gene expression at mRNA level revealed a significant increase in the prefrontal cortex (P˂0.01) but significant decreases in its expressions in the cerebellar cortex (P˂0.01) and the hippocampus (P˂0.05) in rats with hepatic encephalopathy compared to sham control rats. Conclusion: According to the results, it can be concluded that bile duct ligation induces chronic liver failure that in turn leads to hepatic encephalopathy. It can be also proposed that the hypokinesia and other cogniti
