Antier D, Zhang B L, Mailliet F, Akoka S, Pourcelot L, Sannajust F
JE MENESR-1991, Department of Neuropharmacology, Faculty of Pharmacy, 31, Avenue Monge, 37200, Tours, France.
Brain Res. 1998 Oct 5;807(1-2):29-37. doi: 10.1016/s0006-8993(98)00703-3.
The aim of this study was to determine the influence of neonatal focal cerebral hypoxia-ischemia (HI) on sleep-waking pattern, electrocorticogram (ECoG) power spectra and locomotor activity (LA) in adult Wistar rats. Seven-day old pups were subjected to permanent unilateral ligation of the common carotid artery and transient hypoxia (8% O2). At 10 weeks of age, the extent of brain damages was evaluated by magnetic resonance imaging (MRI) and homogenous injured animals were selected before chronic implantation of radiotelemetry device. Using a single ECoG recording channel method, waking (W), paradoxical sleep (PS) and slow wave sleep (SWS) were continuously recorded for 72 h and they were semi-automatically analyzed off-line. We observed that neonatal HI triggers a cascade of events leading, in adult rats, to brain dysfunction characterized by an increase in SWS (55.0 vs. 40.2% in sham-operated rats, p<0.05) and a marked decrease in W phases duration (43.4 vs. 51.5%, p<0.05) while PS was almost suppressed in HI rats (1.6 vs. 8.3%, p<0.05). In addition, power spectral analysis of ECoG revealed significant (p<0.05) alteration in PS power density with a shift of the dominant frequency peak (5.0 to 7.5 Hz for HI and sham-operated rats, respectively). During the light period, we found that HI induced a pronounced reduction of LA (-30%, p<0.05). These results indicate that Wistar rats exposed to a neonatal unilateral cerebral HI present significant ECoG activity, sleep-waking pattern and behavioral disturbances when adults. However, it remains to establish whether such alterations can be prevented by neuroprotective agents.
本研究旨在确定新生期局灶性脑缺氧缺血（HI）对成年Wistar大鼠睡眠-觉醒模式、脑电图（ECoG）功率谱和运动活动（LA）的影响。7日龄幼崽接受永久性单侧颈总动脉结扎和短暂缺氧（8%氧气）处理。在10周龄时，通过磁共振成像（MRI）评估脑损伤程度，并在慢性植入无线电遥测装置之前选择脑损伤均匀的动物。使用单通道ECoG记录方法，连续记录72小时的觉醒（W）、异相睡眠（PS）和慢波睡眠（SWS），并离线进行半自动分析。我们观察到，新生期HI引发一系列事件，导致成年大鼠出现脑功能障碍，其特征为SWS增加（假手术大鼠为40.2%，HI大鼠为55.0%，p<0.05）和W期持续时间显著减少（43.4%对51.5%，p<0.05），而HI大鼠的PS几乎被抑制（1.6%对8.3%，p<0.05）。此外，ECoG的功率谱分析显示PS功率密度有显著（p<0.05）变化，主导频率峰值发生偏移（HI大鼠和假手术大鼠分别从5.0 Hz变为7.5 Hz）。在光照期，我们发现HI导致LA显著降低（-30%，p<0.05）。这些结果表明，暴露于新生期单侧脑HI的Wistar大鼠成年后存在显著的ECoG活动、睡眠-觉醒模式和行为障碍。然而，此类改变是否可通过神经保护剂预防仍有待确定。
