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Social drinkers' performance on tests of abstracting and concept formation declined significantly as a function of age and of the quantity of alcohol consumed per drinking occasion.

Di-n-propylacetate (DPA), a drug known to increase brain gamma-aminobutyric acid (GABA) levels and to inhibit GABA-transamine (GABA-T) activity, was administered during the ethanol withdrawal period to rats made physically dependent upon ethanol. Under all conditions tested, 400 mg DPA/kg injected i.p. significantly reduced the withdrawal hyperexcitable state induced by acoustic stimulation. The effect was seen as early as 30 min after the administration of DPA and lasted for at least 2 hrs. Readministration of the same dose of DPA 6.5 hrs after its initial injection again mitigated withdrawal symptoms. A 200 mg/kg dose of DPA was significantly effective for only 1 hr after its administration. Neither dose led to mortality or observable tranquilization. The results suggest that DPA may be a useful agent in the control of the hyperexcitable state induced by ethanol withdrawal and that the GABA system may be involved in this state.

The effect of ethanol on an enzyme system within an intact functional plasma membrane has been studied using neural cells grown in culture. Rat C6 glioma cells in mono-layer culture were treated acutely or chronically with 100 mM ethanol and the effect of this exposure on the activity of ecto-5'-nucleotidase was determined. Acute exposure led to an increase in enzyme activity with maximum stimulation occurring at concentrations of 100 - 400 mM ethanol. Chronic treatment of cells with 100 mM ethanol for 4 - 8 days also caused an increase in ecto-5'-nucleotidase activity. Both the acute and chronic ethanol-induced stimulation of enzyme activity was completely reversible by removing the ethanol; the acute effects reversed immediately, whereas the chronic effects required several hours. The addition of Concanavalin A demonstrated that the effects on enzyme activity of both chronic and acute exposure to ethanol were blocked by modification of the external cell surface. The effect of chronic exposure to 100 mM ethanol was further localized to an action on the plasma membrane by studies which showed chronic exposure to have no effect on the intracellular 5'-nucleotidase activity. Furthermore, the occurrence of pharmacological tolerance to acute ethanol was observed in this plasma membrane system following chronic treatment of C6 cells with 100 mM ethanol. These findings are consistent with the hypothesis that mammalian neural cells can adapt to the chronic presence of ethanol through changes in their plasma membrane.

Drinking history and sober neuropsychologic performance were examined in 45 male university students between the ages of 21 and 30 yr. Sober performance on the Shipley-Hartford Institute of Living Scale was significantly and inversely related to the amount of alcohol consumed per drinking event. Neither frequency of drinking nor lifetime alcohol consumption were significantly related to cognitive performance in controlled multiple regression equations. These findings emphasize the need for more information about the effects of social drinking on health.

Myelin fractions were prepared from brains of 9- to 90-day-old rats by continuous and discontinuous sucrose density gradient procedures. Total protein and lipid content of myelin showed little variation, but lipid composition changed significantly during maturation. Cholesterol, galactolipids, and ethanolamine glycerophosphatide plasmalogen increased whereas choline glycerophosphatide content decreased with increasing age. The changes in lipid composition were more marked in the myelin prepared by the discontinuous gradient technique. The significance of these lipid changes in relation to their organization in the myelin membrane is discussed.