Brain ethanol, effects

Ethanol Damage and Neuron Loss in the Developing Brain Ethanol Effects on the Developing Brain... 

Alcohol is a socially accepted drug of abuse in Western countries. Due to the high potential for addiction to develop, however, it is actually a hard drug and has a much larger number of victims than the opiate drugs, for example. In the brain, ethanol is deposited in membranes due to its amphipathic properties, and it influences receptors for neurotransmitters (see p. 352). The effect of GABA is enhanced, while that of glutamate declines. 

Drinlciiig alcohol affects the nervous system in five different ways (1 intoxication (loss of physical coordination) (2) niemory U>ss (blackouts amnesia) (3) tolerance (loss of ability to become intoxicated) (4) addiction (uncontrolled craving) and (5) withdrawal symptoms (seizures and tremors) (Diamond and Gordon, 1997), These five effects may all be due to the interaction of ethanol with membrane-bound proteins of the brain. Ethanol is unique among most metabolites, in that it is both water soluble and lipid soluble. Hence, it has the ability to pass directly from the bioodstream into various regions of the brain. 

Heaton, M.B., Paiva, M., Madosky, 1., and Shaw, G. (2003). Ethanol effects on neonatal rat cortex comparative analysis of neurotrophic factors, apoptosis-related proteins, and oxidative processes dining vulnerable and resistant periods. Dev. Brain Res. 145 249-262. 

Opioid systems in the brain are important for the reinforcing effects of ethanol. Selective p-opioid receptor antagonists reliably decrease ethanol drinking in rats. 

The pharmacodynamic effects of ethanol are complex, and any attempt to link its actions to specific neurotransmitters or isolated brain regions is simplistic. A complicated neural network involved in the actions of ethanol accounts for its reinforcing, intoxicating, and abstinence effects. At the present time, use of medications that target neurotransmitters and neuromodulators affected by ethanol represents a reasonable strategy for the development of pharmacotherapies that reduce the reinforcing effects of alcohol and the craving and withdrawal symptoms that commonly occur in the context of alcohol dependence. 

Anton RF, Pettinati H, Zweben A, et al A multi-site dose ranging study of nalmefene in the treatment of alcohol dependence. J Clin Psychopharmacol 24 421 28, 2004 Aragon CM, Stotland LM, Amit Z Studies on ethanol-brain catalase interaction evidence for central ethanol oxidation. Alcohol Clin Exp Res 15 165-169, 1991 Arizzi MN, Correa M, Betz AJ, et al Behavioral effects of intraventricular injections of low doses of ethanol, acetaldehyde, and acetate in rats studies with low and high rate operant schedules. Behav Brain Res 147 203—210, 2003 Azrin NH, Sisson RW, Meyers R, et al Alcoholism treatment by disulfiram and community reinforcement therapy. J Behav Ther Exp Psychiatry 13 105—112, 1982 Babor TF, Kranzler HR, Lauerman RL Social drinking as a health and psychosocial risk factor Anstie s limit revisited, in Recent Developments in Alcoholism, Vol 5. Edited by Galanter M. New York, Plenum, 1987, pp 373 02... 

Montoliu C, ValiJs S, Renau-Piqueras J, Guerri C. Ethanol-induced oxygen radical formation and lipid peroxidation in rat brain effects of chronic alcohol consumption. J Neurochem 1994 63 1855-1862. 

The effects of ethanol on bodily functions, e.g., those of the brain, heart, and liver, are dependent upon the systemic concentrations of ethanol over time. Therefore, the pharmacokinetics of ethanol play a pivotal role in the pharmacodynamic actions of ethanol and of its metabolic product acetaldehyde [6],... 

Once in the blood stream, cocaine levels quickly rise in the brain, faster than plasma levels, which then redistribute to other tissues. Cocaine is rapidly metabolized in the blood and liver, with a half-life of 30 to 90 minutes. The major metabolites have a half-life of approximately 8 hours. Although cocaine itself is detected in urine for only 12 hours, the metabolite benzoylecgonine can be detected in urine for at least 48 hours and sometimes up to 2 weeks. Concurrent use of cocaine and ethanol produces an ethyl ester of benzoylecgonine called cocaethylene. Cocaethylene is an active metabolite, blocking dopamine reuptake, and potentiating the effect of cocaine. Thus, concurrent use of cocaine and ethanol can further increase the additional effects of the drugs and the risk of dependency. 

Rassnick S, Heinrichs SC, Britton KT, Koob GF. 1993. Microinjection of a corticotropin-releasing factor antagonist into the central nucleus of the amygdala reverses anxiogenic-like effects of ethanol withdrawal. Brain Res 605(1) 25-32. 

Robinson DL, Brunner LJ, Gonzales RA. 2002. Effect of gender and estrous cycle on the pharmacokinetics of ethanol in the rat brain. Alcohol Clin Exp Res 26(2) 165-172. 

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