Lesions of the pedunculopontine tegmental nucleus reduce paradoxical sleep (PS) propensity: evidence from a short-term PS deprivation study in rats

Lesions of the pedunculopontine tegmental nucleus reduce paradoxical sleep (PS) propensity: evidence from a short-term PS deprivation study in rats
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DOI:
10.1046/j.0953-816x.2001.01562.x
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发表时间:
2001-05-01
影响因子:
3.4
通讯作者:
Hennevin, E
Hennevin, E
中科院分区:
医学3区
文献类型:
--
作者:
Deurveilher, S;Hennevin, E

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中脑脑桥被盖区的胆碱能神经元被认为在异相睡眠(PS)的产生中起着关键作用。然而,还没有研究检查这些神经元的病变是否会导致大鼠PS的缺陷。我们在这里描述的影响,脚桥被盖核(PPT)病变的自发PS和PS倾向,PS剥夺期间和之后的短时间内表示。通过双侧注射鹅膏蕈氨酸诱导病变。PS剥夺手动进行轻轻唤醒大鼠每次他们表现出PS的多导生理信号。损伤后两周,进行8小时基线记录;第二天,大鼠PS剥夺6小时,然后继续进行多导记录2小时,以检查恢复睡眠。1周后重复相同的方案。与对照组和具有有限PPT病变的大鼠相比,PPT内具有> 60% NADPH-黄递酶阳性细胞损失的大鼠在基线条件下显示不受影响的PS。然而,他们在剥夺期间较少尝试进入PS,并且在剥夺后PS时间表现出衰减的反弹增加。PS尝试的次数和PS反弹的幅度与PPT内心肌黄酶阳性神经元的丢失百分比呈负相关。因此,PS倾向,积累作为PS剥夺的结果减少后,广泛的PPT病变。总之,尽管发现自发PS未改变,但本研究中使用的PS剥夺程序证明了PPT病变引起的PS功能障碍。
Cholinergic neurons in the mesopontine tegmentum are thought to play a critical role in the generation of paradoxical sleep (PS). However, no study has yet examined whether lesions of these neurons cause deficits of PS in the rat. We describe here the effects of lesions of the pedunculopontine tegmental nucleus (PPT) on spontaneous PS and on PS propensity, expressed during and after a short period of PS deprivation. Lesions were induced by bilateral injections of ibotenate. PS deprivation was performed manually by gently waking rats each time they showed polygraphic signs of PS. Two weeks after lesions, an 8-h baseline recording was performed; the following day, rats were PS deprived for 6 h and polygraphic recordings were then continued for 2 h, to examine recovery sleep. The same protocol was repeated 1 week later. Compared with controls and with rats with limited PPT lesions, rats bearing > 60% NADPH-diaphorase-positive cell loss within the PPT showed unaffected PS under baseline conditions. However, they made fewer attempts to enter PS during deprivation and they exhibited an attenuated rebound increase in PS time after deprivation. The number of PS attempts and the magnitude of PS rebound were negatively correlated with the percent loss of diaphorase-positive neurons within the PPT. Thus, PS propensity that accumulated as a result of PS deprivation was reduced after extensive PPT lesions. In summary, although spontaneous PS was found to be unaltered, the PS deprivation procedure used in this study demonstrated the dysfunctioning of PS caused by PPT lesions.