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作 者:Dinesh Pal Vibha Madan Birendra Nath Mallick
机构地区:[1]Jawaharlal Nehru大学生命科学学院,印度新德里110067
出 处:《生理学报》2005年第4期401-413,共13页Acta Physiologica Sinica
基 金:This work was supported by Fund from CSIR, DBT, DST, ICMR and UGC, India.
摘 要:两种类型的神经元参与了快速眼动(rapideyemovement,REM)睡眠的调节:快速眼动-发放(REM-ON)神经元和快速眼动-沉寂神经元(REM-OFF)。快速眼动-沉寂神经元属去甲肾上腺素能神经元,正如名字表示的那样——在快速眼动睡眠期间停止发放。已有研究表明,这些神经元放电活动的停止是导致快速眼动睡眠的前提条件,γ-氨基丁酸(γ-aminobutyricacid,GABA)可使它们停止发放。如果这些神经元不停止发放,脑中的去甲肾上腺素水平将升高,不出现快速眼动睡眠。剥夺快速眼动睡眠所引起的去甲肾上腺素增加,至少是快速眼动睡眠丧失引起Na+-K+ATP酶活性增加的原因,而这可能是导致快速眼动睡眠剥夺所引发的各种效应的主要因素。Two types of neurons are involved in the regulation of rapid eye movement (REM) sleep, the REM-ON and the REM-OFF neurons. As the name suggests, the REM-OFF neurons cease firing during REM sleep and they are norepinephrinergic. It has been shown that cessation of these neurons is a pre-requisite for the generation of REM sleep and GABA shuts them off. Further, if these neurons do not shut off, there is increased levels of norepinephrine in the brain and loss of REM sleep. The REM sleep deprivation induced increase in norepinephrine is responsible for mediating at least REM sleep loss induced increase in Na^+-K^+ ATPase activity,which is likely to be tile primary factor for causing REM sleep deprivation induced effects.
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