The importance of sleep in physiological functioning has attracted scientific research for more than two decades. A variety of processes have now been discovered to require adequate sleep for ideal functioning including memory consolidation. While abundant research is available on the role of hippocampal neuronal activities in these processes as we sleep, it is important to consider the role of the more abundant neuronal counterparts in the Central Nervous System (CNS), the glia. Glial cells, especially astrocytes, have recently been established as an essential component of the process of long-term depression (LTD) as well as mediators of long-term potentiation (LTP), both of which are essential cellular correlated of memory. Given their important role in memory consolidation, it is not surprising that sleep deprivation (SD) may mediate some of its negative impacts on memory through glial cells. The following review discusses various glial factors that may explain how SD alters glial processes of memory, namely its effects on adenosine, Nitric Oxide (NO) and the metabolism of energy in the brain. Moreover, emerging research on the effects of Brain Fatty Acid Binding Protein (FABP7) and cell proliferation within the hippocampus following SD is also discussed. However, given the abundance of changes observed in glial cells following SD, it is likely that these factors make up only a proportion of the overall influence that glial cells may have on memory following SD. Furthermore, a lack of available human research as well as a difference of methodologies employed for achieving SD in an experimental setting demand a better approach for advancing our knowledge of the role of SD in altering the various glial processes that play a role in memory consolidation. Based on the possibility of a connection that may exist between the various species of animals discussed, it is suggested that these connections be considered for future research.