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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 20 (2004), S. 0 
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The Edinger–Westphal nucleus (EW) is a brain region that has recently been implicated as an important novel neural target for ethanol. Thus, the EW is the only brain region consistently showing elevated c-Fos expression following both voluntary and involuntary ethanol administration. Ethanol-induced c-Fos expression in the EW has been shown to occur in urocortin I-positive neurons. Moreover, previous reports using several genetic models have demonstrated that differences in the EW urocortin I system are correlated with ethanol-mediated behaviours such as ethanol-induced hypothermia and ethanol consumption. The aim of this study was to confirm these relationships using a more direct strategy. Thus, ethanol responses were measured following electrolytic lesions of the EW in male C57BL/6J mice. Both EW-lesioned and sham-operated animals were tested for several ethanol sensitivity measures and ethanol consumption in a two-bottle choice test. The results show that lesions of the EW significantly disrupted ethanol-induced hypothermia, while having no effect on pupillary dilation, locomotor activity or ethanol-induced sedation. In addition, EW-lesioned animals showed significantly lower ethanol preference and total ethanol dose consumed in the two-bottle choice test. EW-lesioned animals also consumed less sucrose than sham-operated animals, but did not have altered preferences for sucrose or quinine in a two-bottle choice test. These data support previously observed genetic correlations between EW urocortin I expression and both ethanol-induced hypothermia and ethanol consumption. Taken together, the findings suggest that the EW may function as a sensor for ethanol, which can influence ethanol consumption and preference.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 139 (1998), S. 34-43 
    ISSN: 1432-2072
    Keywords: Key words Ethanol ; Amnesia ; Learning ; Immediate early gene ; Hippocampus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Acute alcohol intoxication disrupts memory acquisition in humans and laboratory animals. This review summarizes recent behavioral and immediate early gene expression studies addressing the mechanisms of this phenomenon. Most behavioral investigations agree that the amnestic effect of alcohol is due to its preferential detrimental effect on hippocampus-dependent than on hippocampus-independent forms of learning. However, some hippocampal lesion studies contradict these results. Learning in behavioral paradigms is accompanied by induction of c-fos and other immediate early genes in many brain regions of the animal. In contrast, studies on alcohol-mediated changes in expression of this gene confirm selective hippocampal suppression of basal and experience-induced expression of c-fos after acute and repeated administration of alcohol. This hippocampal suppression is in marked contrast with alcohol-mediated induction of c-fos expression in other brain areas. However, the selective suppression of hippocampal gene expression and memory by alcohol is most likely mediated by a number of interacting neurotransmitter systems. Thus, effects of lower doses of alcohol (0.5 g/kg or lower in rats) seem to be preferentially mediated through GABAergic systems. At intermediate doses (0.75–2 g/kg), several other neurotransmitter systems are affected besides GABA. Higher doses lead to none-specific effects, probably involving even more neurotransmitter systems. Elucidation of these neurotransmitter systems will be highly important for developing rational approaches for correction of alcohol-related cognitive disorders.
    Type of Medium: Electronic Resource
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