The effect of memantine on cerebral cortex tumor necrosis factor alpha exression in a rat model of acute hyperammonemia

Background Literature suggests that proinflammatory mechanisms are implicated in the pathophysiology of hepatic encephalopathy. This is mainly caused by high circulating levels of ammonia (hyperammonemia-HA), due to liver failure [1,2]. In addition, NMDA receptors are excessively activated during acute hyperammonemia and thus significally contribute to the brain damage [3]. In fact, blockage of this receptor type is beneficial in experimental models of acute hyperammonemia [3,4]. The aim of this study is to assess the effect of memantine, a noncompetitive NMDA receptor antagonist, on the expression of tumor necrosis factor alpha (TNF-a), a major proinflammatory cytokine, in the brain of a rat model of acute hyperammonemia.