Effects of Acute and Chronic Ethanol Administration on the Poly-Phosphoinositide Signaling Activity in Brain
Ethanol ingestion is known to exert diverse physiological effects on many body organs including the central nervous system (CNS). While excess acute ethanol intake can result in sedation, chronic ingestion is associated with development of tolerance and physical dependence and in turn, this may lead to the manifestation of withdrawal hyperexcitability. The biochemical mechanisms underlying the effects of ethanol are not well understood although alterations of many cell surface processes including membrane transport enzymes, receptors and ion channel activities have been implicated (see review by Deitrich et al., 1989). Some of these effects may be due partly to ethanol’s ability to disorder membrane lipids, resulting in an alteration of the intricate relationship between proteins and lipids within the membrane. However, it is clear that ethanol does not act globally on the membrane lipids, rather, changes are attributed to the effects of ethanol on specific types of lipids present in different membrane domains (Wood and Schroeder, 1988). In order to better understand the physiological manifestations related to acute and chronic ethanol ingestion, it is important first to identify the ethanol-sensitive biochemical mechanisms in brain and then followed by attempts to understand how adaptation to the changes is developed.
KeywordsHydrolysis Sucrose Ischemia Lithium Serotonin
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