Abstract
Considerable progress has been made in recent years toward understanding the neurochemical events occurring in hepatic encephalopathy (HE). However, an integrated picture of all of the available facts and events regarding the pathogenesis of this condition has yet to emerge. Many studies to date have largely ignored certain fundamental cellular changes which occur in this condition. In this article, the involvement of astrocytes in HE will be reviewed in an attempt to bridge this gap in our knowledge. Studies carried out in our laboratory on astrocytes dealing with the effect of ammonia and other putative toxins will be presented, and an attempt will be made to integrate these findings with current pathogenetic views of HE. New concepts dealing with the role of second messengers and protein phosphorylation will be presented. Finally, we wish to leave the reader with the concept that HE represents a primary gliopathy, i.e., that the astrocyte is the prime CNS target in HE.