Sleep deprivation increases A(1) adenosine receptor density in the rat brain.

Sleep deprivation increases A(1) adenosine receptor density in the rat brain.
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睡眠剥夺增加了大鼠脑中的A(1)腺苷受体密度。

DOI:
10.1016/j.brainres.2008.12.056
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发表时间:
2009-03-03
期刊:
影响因子:
2.9
通讯作者:
Bauer A
Bauer A
中科院分区:
医学3区
文献类型:
--
作者:
Elmenhorst D;Basheer R;McCarley RW;Bauer A

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腺苷在睡眠剥夺后增加,并通过A1腺苷受体(A1AR)起作用,可能是睡眠稳态控制的关键因素。本研究利用[3H]CPFPX放射自显影技术研究了睡眠剥夺对大鼠大脑不同部位A1AR密度的影响。与未受昼夜睡眠-觉醒节律干扰的对照组相比,睡眠剥夺24小时后,顶叶皮层(PAR)(7%)、丘脑(11%)和尾状壳核(9%)的[3H]CPFPX结合显著增加。与昼夜节律对照组相比,12小时的睡眠剥夺使受体密度在- 5%至+9%之间(运动皮层(M1),有统计学意义)发生了区域性变化。这些结果表明大脑a1ar参与了睡眠剥夺和睡眠调节的影响。A1AR密度的增加不仅可以维持对腺苷水平升高的反应性,还可以放大睡眠剥夺的影响,并且与睡眠诱导的突触水平的内稳态重组相一致。
Adenosine, increasing after sleep deprivation and acting via the A1 adenosine receptor (A1AR), is likely a key factor in the homeostatic control of sleep. This study examines the impact of sleep deprivation on A1AR density in different parts of the rat brain with [3H]CPFPX autoradiography. Binding of [3H]CPFPX was significantly increased in parietal cortex (PAR) (7%), thalamus (11%) and caudate-putamen (9%) after 24 h of sleep deprivation compared to a control group with an undisturbed circadian sleep-wake rhythm. Sleep deprivation of 12 h changed receptor density regionally between −5% and +9% (motor cortex (M1), statistically significant) compared to the circadian control group. These results suggest cerebral A1ARs are involved in effects of sleep deprivation and the regulation of sleep. The increase of A1AR density could serve the purpose of not only maintaining the responsiveness to increased adenosine levels but also amplifying the effect of sleep deprivation and is in line with a sleep-induced homoeostatic reorganization at the synaptic level.
DOI: 10.1016/s0169-328x(99)00219-3
发表时间: 1999-11-10
期刊: MOLECULAR BRAIN RESEARCH
影响因子: --
作者:
Basheer, R;Porkka-Heiskanen, T;McCarley, RW
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