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  • 1
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Primary hippocampal neuronal cultures exhibited a concentration- and time-dependent loss of cells when exposed to ethanol (EtOH). EtOH-induced neurotoxicity was attenuated by 2,4-dimethoxybenzilidene anabaseine (DMXB) which selectively activates alpha7 nicotinic receptors in a concentration-dependent manner. We further investigated the mechanisms of the protective effect of DMXB on EtOH- induced neurotoxicity. We found that EtOH decreased the mitochondrial membrane potential and released cytochrome c from mitochondria at neurotoxic concentrations. DMXB (3 μm) attenuated both of these actions in a manner that was in turn blocked with the nicotinic antagonist methyllyconitine (MLA) 100 nm. Neither DMXB nor MLA alone affected these parameters. These results suggest that the neuroprotection conferred by alpha7 nicotinic receptor activation may be mediated, at least in part, through preventing the decrease in the mitochondrial membrane potential and the increase in the release of cytochrome c caused by EtOH.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 22 (1971), S. 45-49 
    ISSN: 1432-2072
    Keywords: Alcohol ; Withdrawal ; Seizures ; Audiogenic
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract An ethanol withdrawal syndrome, consisting of tremors and convulsions, was induced in C57BL/6J mice by feeding them a liquid diet containing 27% of ethanol-derived calories at an environmental temperature of +12 to 13° C for 6 days. Control groups were pair-fed with liquid diets containing isocaloric amounts of sucrose or Laboratory Chow. Seven and 24 h after the beginning of withdrawal, all mice were exposed to bell ringing for 90 sec. This sound induced convulsions in nearly one-half of ethanol-consuming mice at 7 h and in a few mice at 25 h. Only one mouse of the control groups had a convulsion. These findings support the concept that the ethanol withdrawal syndrome is a partially latent state of hyperexcitability of the brain following depression by ethanol.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 56 (1978), S. 287-292 
    ISSN: 1432-2072
    Keywords: Ethanol dependence ; Ethanol withdrawal ; Ethanol withdrawal syndrome
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Electrodes were chronically implanted in the dorsal hippocampus of rats. Pretreatment levels of neural excitability were assessed by determining the duration of direct hippocampal electrical stimulation sufficient to induce forelimb clonus in each rat. Following baseline measurements the rats were administered an alcohol or sucrose-containing liquid diet and 19–22 days later were withdrawn. Two postwithdrawal stimulation sessions were conducted on each animal. Separate groups of ethanol-dependent and control rats were given primary stimulation sessions at 8 h, 24 h, 72 h, or 1 week postwithdrawal. Secondary stimulation sessions were conducted 1 week or 2 weeks postwithdrawal. The results from the primary stimulations indicated that ethanol-dependent animals exhibited significant neural hyperexcitability for at least 72 h, but not 1 week, postwithdrawal. Results from the secondary stimulations demonstrated the presence of a relative neural hypoexcitability in ethanol-dependent groups as compared to controls. The pattern of results suggests, however, that the observed relative neural hypoexcitability was not the direct result of ethanol withdrawal.
    Type of Medium: Electronic Resource
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