Hypoxia inducible factor-1 influences sensitivity to paclitaxel of human lung cancer cell lines under normoxic conditions
- 作者：Li Hua Zeng ; Guo Zhen Guo ; Shinae Kizaka-Kondoh ; Satoshi Itasaka ; Masahiro Hiraoka
- 关键词：amygdala ; open field ; REM ; synaptic plasticity ; Rim1
//www.sciencedirect.com/scidirimg/entities/204e.gif" alt="greek small letter alpha" title="greek small letter alpha" border="0">KO
- 刊名：Cell Biology International
- 出版年：2008
- 期刊代码：164_10656995
- 类别：bio
- 出版时间：March 2008
- 卷：32
- 期：3
- 页码：S38
- 文件大小：44 K
摘要
Sleep mechanisms and synaptic plasticity are thought to interact to regulate homeostasis and memory formation. However, the influences of molecules that mediate synaptic plasticity on sleep are not well understood. In this study we demonstrate that mice lacking Rab3 interacting molecule 1 alpha (RIM1
) (Rim1KO), a protein of the synaptic active zone required for certain types of synaptic plasticity and learning, had 53±5%less baseline rapid eye movement (REM) sleep compared with their wild type littermates. Also, compared with wild type littermates, exposure of the mice to an open field or to a novel object induced more robust and longer lasting locomotion suggesting altered habituation. This difference in exploratory behavior correlated with genotype specific changes in REM and deregulated release of norepinephrine in the cortex and basal amygdala of the Rim1KO mice. Also, moderate sleep deprivation (4 h), a test of the homeostatic sleep response, induced REM sleep rebound with different time course in Rim1KO and their wild type littermates. As norepinephrine plays an important role in regulating arousal and REM sleep, our data suggest that noradrenergic deficiency in Rim1KO animals impacts exploratory behavior and sleep regulation and contributes to impairments in learning.
) (Rim1KO), a protein of the synaptic active zone required for certain types of synaptic plasticity and learning, had 53±5%less baseline rapid eye movement (REM) sleep compared with their wild type littermates. Also, compared with wild type littermates, exposure of the mice to an open field or to a novel object induced more robust and longer lasting locomotion suggesting altered habituation. This difference in exploratory behavior correlated with genotype specific changes in REM and deregulated release of norepinephrine in the cortex and basal amygdala of the Rim1KO mice. Also, moderate sleep deprivation (4 h), a test of the homeostatic sleep response, induced REM sleep rebound with different time course in Rim1KO and their wild type littermates. As norepinephrine plays an important role in regulating arousal and REM sleep, our data suggest that noradrenergic deficiency in Rim1KO animals impacts exploratory behavior and sleep regulation and contributes to impairments in learning.