Acute or chronic liver failure leads to alterations in the central nervous system functions, in what has been defined as hepatic encephalopathy. This term comprises neurological alterations that range from discrete changes in personality to confusion and coma. The neurochemical framework of this syndrome is the deregulation of neurotransmission without a significant neuronal death. In contrast, astrocyte swelling, and activation of microglia are exacerbated. As glutamate is the major excitatory neurotransmission system in the vertebrate brain, it is not surprising that the metabolism and recycling of this transmitter are compromised in acute liver failure. Moreover, liver glutamate handling is regulated by the same group of plasma membrane transporters expressed in glia cells. Therefore, the components of the so-called glutamate/glutamine shuttle are attractive targets for plausible intervention in hepatic encephalopathy.

This Research Topic focuses on the role of glutamate transporters in brain and liver pathologies. Our main objective is to improve understanding of the molecular mechanisms and the impact of differential gene expression patterns of these proteins in the etiology of hepatic failure.

Current knowledge will be analyzed in terms of the parallelism of brain and liver damage. Special attention will be placed on glutamate and glutamine transporters, their structure, function, and gene expression regulation in the healthy and diseased liver. We welcome Original Research, Reviews and Mini-Review articles based on the following topics:

• Regulation of the expression of glutamate and glutamine transporter genes;

• Glutamate and glutamine turnover in the liver and brain;

• Glutamate and glutamine transporters as signaling proteins;

• Glutamate and glutamine transporters in cancer;

• GABA/Glutamate and glutamine an ammonia metabolism: the brain liver connection.

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Frontiers in Endocrinology

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