دانلود مقاله ISI انگلیسی شماره 156872
ترجمه فارسی عنوان مقاله

داروهای ضد افسردگی در طول بوی عود: اثرات فلو تریزپام، زولپیدم و اسکاپولامین

عنوان انگلیسی
Amnestic drugs in the odor span task: Effects of flunitrazepam, zolpidem and scopolamine
کد مقاله سال انتشار تعداد صفحات مقاله انگلیسی
156872 2017 8 صفحه PDF
منبع

Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)

Journal : Neurobiology of Learning and Memory, Volume 145, November 2017, Pages 67-74

پیش نمایش مقاله
پیش نمایش مقاله  داروهای ضد افسردگی در طول بوی عود: اثرات فلو تریزپام، زولپیدم و اسکاپولامین

چکیده انگلیسی

The odor span task is an incrementing non-matching–to-sample procedure designed to provide an analysis of working memory capacity in rodents. The procedure takes place in an arena apparatus and rats are exposed to a series of odor stimuli in the form of scented lids with the selection of new stimuli reinforced. This procedure makes it possible to study drug effects as a function of the number of stimuli to remember. In the present study, the non-selective positive allosteric GABAA receptor modulator flunitrazepam impaired odor span performance at doses that did not affect a control odor discrimination. In contrast, the alpha-1 selective positive GABAA receptor modulator zolpidem and the cholinergic receptor antagonist scopolamine only impaired odor span at doses that produced more global impairment, including decreased accuracy in the control discrimination and increased response omissions in the both the odor span and control discrimination procedures. Even though the effects of flunitrazepam were selective to odor span performance, they did not depend on the number of stimuli to remember—the same degree of impairment occurred regardless of the memory load. These findings suggest that flunitrazepam interfered selectively with conditional discrimination performance rather than working memory and tentatively suggest that flunitrazepam’s selective effects in the odor span task relative to the control odor discrimination are mediated by one or more non-alpha1 GABAA receptor subtypes.