Synaptosomal membrane lipids of mice during continuous exposure to ethanol

Littleton, J M; John, G. R.

doi:10.1111/j.2042-7158.1977.tb11407.x

Cited by 165 publications

(24 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Studies have shown that EtOH is likely to be found on the hydrophilic membrane surface or in protein pockets (Barry and Gawrisch, 1994;Chiou et al, 1992;Hitzeman et al, 1986;Klemm, 1998;Moxon et al, 1991;Rottenberg, 1987Rottenberg, , 1992 or, less likely, in the core of biological membranes, which show a relatively low partition coefficient for short chain alcohols such as EtOH (Barry and Gawrisch, 1994;Chiou et al, 1992;Klemm, 1998;Metcalfe et al, 1968;Rottenberg, 1992). The amount of macromoleculeassociated EtOH in membranes has been described to range from 6% to 90%, depending on the type of membrane investigated (Grenell, 1975;Kelly-Murphy et al, 1984;Nie et al, 1989;Rottenberg et al, 1981;Sarasua et al, 1989), and to be affected by chronic alcohol exposure (Beauge et al, 1985;Chin and Goldstein, 1977;Kelly-Murphy et al, 1984;Littleton and John, 1977;Rottenberg et al, 1981Rottenberg et al, , 1987Sarasua et al, 1989;Wood et al, 1987;reviewed in Rottenberg, 1992). The EtOH molecules in any of these molecular environments are restricted motionally, so that their T 2 relaxation times are extremely short (<1 msec).…”

Section: Relaxationmentioning

confidence: 99%

Ethanol in Human Brain by Magnetic Resonance Spectroscopy: Correlation With Blood and Breath Levels, Relaxation, and Magnetization Transfer

Fein

Meyerhoff

2000

Alcoholism: Clinical and Experimental Research

View full text Add to dashboard Cite

Background-Proton magnetic resonance spectroscopy ( 1 H MRS) allows measurement of alcohol in the human brain after alcohol consumption. However, the quantity of alcohol that can be detected in the brain by 1 H MRS pulse sequences has been controversial, with values ranging from about 24% to 94% of the temporally concordant blood alcohol concentrations. The quantitation of brain alcohol is critically affected by the kinetics of alcohol uptake and elimination, by the relaxation times of the protons that give rise to the brain alcohol signal, and by the specifics of both pulse sequence timing and radio frequency pulse applications.

show abstract

Section: Relaxationmentioning

confidence: 99%

Ethanol in Human Brain by Magnetic Resonance Spectroscopy: Correlation With Blood and Breath Levels, Relaxation, and Magnetization Transfer

Fein

Meyerhoff

2000

Alcoholism: Clinical and Experimental Research

View full text Add to dashboard Cite

show abstract

“…Ethanol is believed to intercalate into cell membranes, producing acute and adaptive changes in membrane fluidity (1, 2) or membrane constituents (3,4). Adenosine receptors are membrane-bound proteins that appear to mediate some of the effects of ethanol in the central nervous system (5).…”

Section: Introductionmentioning

confidence: 99%

Basal and adenosine receptor-stimulated levels of cAMP are reduced in lymphocytes from alcoholic patients.

Diamond¹,

Wrubel²,

Estrin³

et al. 1987

Proc. Natl. Acad. Sci. U.S.A.

140

View full text Add to dashboard Cite

Alcoholism causes serious neurologic disease that may be due, in part, to the ability of ethanol to interact with neural cell membranes and change neuronal function. Adenosine receptors are membrane-bound proteins that appear to mediate some of the effects of ethanol in the brain. Human lymphocytes also have adenosine receptors, and their activation causes increases in cAMP levels. To test the hypothesis that basal and adenosine receptor-stimulated cAMP levels in lymphocytes might be abnormal in alcoholism, we studied lymphocytes from 10 alcoholic subjects, 10 age-and sexmatched normal individuals, and 10 patients with nonalcoholic liver disease. Basal and adenosine receptor-stimulated cAMP levels were reduced 75% in lymphocytes from alcoholic subjects. Also, there was a 76% reduction in ethanol stimulation of cAMP accumulation in lymphocytes from alcoholics. Similar results were demonstrable in isolated T cells. Unlike other laboratory tests examined, these measurements appeared to distinguish alcoholics from normal subjects and from patients with nonalcoholic liver disease. Reduced basal and adenosine receptor-stimulated levels of cAMP in lymphocytes from alcoholics may reflect a change in cell membranes due either to chronic alcohol abuse or to a genetic predisposition unique to alcoholic subjects.Despite the widespread incidence of alcoholism, the molecular events accounting for intoxication, tolerance, and physical dependence after alcohol abuse are poorly understood. Ethanol is believed to intercalate into cell membranes, producing acute and adaptive changes in membrane fluidity (1, 2) or membrane constituents (3,4). Adenosine receptors are membrane-bound proteins that appear to mediate some of the effects of ethanol in the central nervous system (5). We recently reported (6) that ethanol acutely increases adenosine receptor-stimulated cAMP levels in a clonal neural cell line (neuroblastoma-glioma hybrid and that with time these cells adapt to the presence of ethanol, showing a reduction in adenosine receptor-stimulated cAMP levels. After chronic exposure to ethanol, the NG108-15 cells require ethanol to achieve normal levels of adenosine receptorstimulated cAMP, which may indicate a form of cellular "dependence." This process is completely reversible upon ethanol withdrawal.These observations suggest that intact single cells adapt to the presence of ethanol. Moreover, depressed adenosine receptor-stimulated cAMP levels in cells might be a biochemical change of pathophysiologic significance in chronic alcoholism. Since human lymphocytes have the same A2 adenosine receptors as the neuroblastoma cells (7), we could test directly whether alcoholics have altered cAMP levels. We undertook a controlled study of basal and adenosine receptor-stimulated cAMP levels in lymphocytes of chronic alcoholics, normal subjects, and patients with nonalcoholic liver disease. Mixed lymphocytes and T cells from chronic alcoholics showed a striking reduction in basal and adenosine receptor-stimulated cAMP levels. Moreov...

show abstract

“…However, unlike the microsomal membranes, the myelin membrane fraction from the ethanol-treated animals showed a decrease in cholesterol (Moscatelli and Demediuk, 1980). Finally, the fatty acid composition of lipids in crude brain synaptosomal membranes and in mitochondrial and synaptic membranes obtained from mice that were maintained for 10 days on ethanol inhalation showed a significant increase in 18: 0 and a significant decrease in 20: 4 fatty acids (Littleton, 1977;Littleton et aI., 1980). Although some changes in synaptosomal fatty acids did not reach levels of significance, they did show a trend similar to that observed for liver mitochondria, such as the approximately 30% decrease in 18: 2 fatty acids (Littleton, 1977).…”

Section: Chemical Effects: Acute and Chronic Ethanol Effects On The Cmentioning

confidence: 94%

Physico-Chemical Interactions between Alcohol and Biological Membranes

Michaelis

1983

Research Advances in Alcohol and Drug Problems

View full text Add to dashboard Cite

Synaptosomal membrane lipids of mice during continuous exposure to ethanol

Cited by 165 publications

References 7 publications

Ethanol in Human Brain by Magnetic Resonance Spectroscopy: Correlation With Blood and Breath Levels, Relaxation, and Magnetization Transfer

Ethanol in Human Brain by Magnetic Resonance Spectroscopy: Correlation With Blood and Breath Levels, Relaxation, and Magnetization Transfer

Basal and adenosine receptor-stimulated levels of cAMP are reduced in lymphocytes from alcoholic patients.

Physico-Chemical Interactions between Alcohol and Biological Membranes

Contact Info

Product

Resources

About