Alcoholism, clinical and experimental research
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Alcohol. Clin. Exp. Res. · Feb 1999
Clinical TrialThe role of somatic disorders and physical injury in the development and course of alcohol withdrawal delirium.
In a retrospective study, we evaluated the role of somatic disease and physical injury in the development and course of alcohol withdrawal delirium. Medical records of 1179 patients treated for alcohol withdrawal in Nowowiejski Hospital in Warsaw from 1973 to 1987 were reviewed using a structured questionnaire. Development, symptoms' severity, and the course of alcohol withdrawal delirium were assessed in possible relation to the somatic state of patients and other variables of alcohol dependence. ⋯ Early development and severe course of alcohol withdrawal delirium correlated with the late beginning of excessive drinking (over the age of 40) and concomitant abuse of benzodiazepines or barbiturates. We concluded that somatic disorders or physical injury might trigger delirium during alcohol withdrawal, and have essential influence on the symptoms' severity and duration of DT. A more severe course of DT is also correlated with the quantity of alcohol consumed and concomitant abuse of sedatives.
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Alcohol. Clin. Exp. Res. · Feb 1999
Comparative StudyChronic ethanol upregulates NMDA and AMPA, but not kainate receptor subunit proteins in rat primary cortical cultures.
The present study examined the effects of chronic ethanol exposure on the expression of N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxalone (AMPA) and kainate receptor subunit proteins in rat cortical neuronal cultures grown in media containing 2 mM (high) or 0.1 mM (low) glutamine. Immunoblot analysis of NMDA (NR1, NR2A, NR2B, and NR2D), AMPA (GluR1 and GluR2/3), and kainate (GluR6/7) subunit polypeptides in 3-, 5-, 8-, 10-, and 12 day-old-cultures showed that NMDA receptor subunits NR1, NR2A, and NR2B and AMPA receptor subunits GluR2/3 progressively increased as a function of time, whereas levels of NMDA subunit NR2D were high at day 3 and progressively declined to barely detectable levels by day 12. Levels of AMPA subunit GluR1 and the kainate subunit GluR6/7 remained stable throughout the time course. ⋯ In contrast, chronic ethanol did not alter the levels of any of these subunit proteins in cells grown in high glutamine. These data demonstrate that under certain experimental conditions, prolonged exposure to ethanol upregulates NMDA and AMPA receptor subunit proteins, but has no effect upon kainate receptor subunit proteins. Because we have previously shown that acute ethanol can inhibit NMDA and AMPA, but not kainate, receptor function in these cultures, the increase in subunit expression likely reflects an adaptive response to the inhibitory effects of ethanol and suggests that both NMDA and AMPA receptors may play an important role in adaptation of the CNS to chronic ethanol.