Search In this Thesis
   Search In this Thesis  
العنوان
Role of brain derived neurotrophic factor and oxidative stress in memory dysfunction in rapid eye movement sleep deprived rats /
المؤلف
Elsayed, Noha Mohamed Badae.
هيئة الاعداد
باحث / نهى محمد بديع السيد
مشرف / على خليل على السيد
مشرف / علاء الدين حسن محمود
مشرف / هالة صلاح إبراهيم
الموضوع
Medical Physiology.
تاريخ النشر
2014.
عدد الصفحات
p111. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الطب
تاريخ الإجازة
3/4/2014
مكان الإجازة
جامعة الاسكندريه - كلية الطب - Medical Physiology
الفهرس
Only 14 pages are availabe for public view

from 153

from 153

Abstract

Sleep is defined as a natural and reversible state of reduced responsiveness to external stimuli and relative inactivity, which is important for the maintenance of physiological homeostasis and psychological balance. Among the multiple functions of sleep, its role in the establishment of memories seems to be particularly important. Sleep has been shown to promote primarily the consolidation of memory. Previous studies in rats and humans aiming to determine whether different sleep stages have different roles in memory consolidation, mainly focused on rapid eye movement (REM) sleep and the consequences of REM sleep deprivation (REMSD). REM sleep was shown to increase after learning a certain task during specific time periods dependent on the task. In the Morris water maze task, it started more than 2 h after learning and persisted for 22 h. The increase in REM sleep during the specific time periods predicted later memory recall, whereas selective deprivation of REM sleep during these time periods was shown to impair memory.
Memory is composed of several stages including acquisition, consolidation (retention) and retrieval. Acquisition is the step during which a task is learnt, consolidation is the process during which the memory is stabilized, and retrieval is the bringing back of the learned task. These three stages of memory can be tested in experimental animals using water maze task.
Memory consolidation involves the strengthening of memory representations through anatomical changes at the synaptic level (synaptic consolidation).Long-term potentiation (LTP) is considered a major mechanism of synaptic consolidation that is induced in the hippocampus during REM sleep. REM sleep has been shown to mediate the expression of plasticity-related immediate early genes (IEGs) like activity regulated cytoskeleton associated protein (Arc), Early growth response protein 1 (Egr1) and brain derived neurotrophic factor (BDNF) through hippocampal LTP. Of those, BDNF is especially considered a key protein involved in hippocampal synaptic plasticity. It participates in multiple forms of learning and memory formation.
The aim of the present work was to assess the effect of REMSD on memory consolidation and to investigate the role BDNF in memory impairment of REM sleep deprived rats, and the possible effect of oxidative stress and apoptosis as underlying mechanisms.
This study was conducted on 48 adult male albino rats (200-250 g) which were divided into 3 main equal groups and each group was further subdivided into 2 subgroups:-
Group Ι: It included 16 rats (stress-control animals), this group wasn’t sleep deprived. They were placed on large platforms in the water pool allowing them to sleep on it.
Subgroup ΙA: Included 8 rats allowed to sleep on large platforms for 3 days.
Subgroup ΙB: Included 8 rats allowed to sleep on large platforms for 6 days.
Group ІІ: It included 16 rats that were subjected