In cirrhosis, some toxic substances accumulate in the brain and modify its functional integrity. In this study, we investigate the impacts of liver damage on the neuronal profile of the prefrontal cortex (PFC) in a rat model of hepatic damage induced with carbon tetrachloride (CCl4). This study also evaluated the possible role of liver dysfunction in the etiology of neurodegenerative characteristics associated with the PFC. Ten male Wistar rats weighing 120 to 190 g body weight were used for this study. The rats were divided into 2 groups (A and B) of 5 rats each. The rats in group A (control group) were treated with phosphate buffered saline (PBS) solution only while the rats in group B (treatment group) were treated with carbon tetrachloride (CCl4). The prefrontal cortices of the rats were excised from skulls of the rats, fixed in formol calcium, while the livers were excised from the abdomen of the rats and were fixed in formol saline for cytoarchitectural study using Cresyl fast violet and hematoxylin and eosin stains respectively. The main neuropathological findings observed in this study include cortical necrosis, uneven neuronal loss with varying range of vacuolations in the prefrontal cortices of the CCl4 treated rats when compared with the PBS treated rats. It was observed that the administration of CCl4 induces changes in hepatocellular morphology of the treated rats and these include moderate vascular congestion and extensive cytoplasmic damage in the hepatocytes. These results could be due to loss of hepatic functions.
Key words: Liver damage, neuropathology, neurons, prefrontal cortex, rat.
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