Abstract
Alcohol ingestion by man is known to produce well recognized effects on the central nervous system (CNS). While excessive drinking is associated with intoxication, chronic ethanol ingestion may result in the manifestations of tolerance and physical dependence. The central depressant effect of acute ethanol is associated with an inhibition of neuronal firing and suppression of neurotransmitter release. Ethanol can be regarded as an anesthetic compound (38); however, due to its high water solubility, the anesthetic potency of ethanol is very weak and a high concentration is required for nerve blocking activity. Although tolerance and physical dependence associated with chronic ethanol ingestion can be attributed largely to alterations of the neuronal membrane, the complex structural and functional organization of the brain has prevented biochemists to elucidate these events at the molecular level. In recent years, much effort has been devoted to examining the ethanol effects on various neurotransmitter systems (see review in reference 32), yet, these studies have not been able to arrive at a conclusion to discern whether or not ethanol acts preferentially on a particular neurotransmitter system.
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Sun, G.Y., Chandrasekhar, R., Huang, HM. (1989). Effects of Acute and Chronic Ethanol Administration on Metabolism of Brain Acidic Phospholipids. In: Sun, G.Y., Rudeen, P.K., Wood, W.G., Wei, YH., Sun, A.Y. (eds) Molecular Mechanisms of Alcohol. Experimental Biology and Medicine, vol 21. Humana Press. https://doi.org/10.1007/978-1-4612-4514-8_2
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DOI: https://doi.org/10.1007/978-1-4612-4514-8_2
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