Extradural compression of sensorimotor cortex: a useful model for studies on ischemic brain damage and neuroprotection.

Extradural compression of sensorimotor cortex: a useful model for studies on ischemic brain damage and neuroprotection.
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感觉运动皮层的硬膜外压缩:研究缺血性脑损伤和神经保护的有用模型。

DOI:
10.1089/089771502753460259
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发表时间:
2002
影响因子:
4.2
通讯作者:
S. Liljequist
S. Liljequist
中科院分区:
医学2区
文献类型:
--
作者:
Jurgita Kundrotiené;A. Wägner;S. Liljequist

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对Sprague-Dawley大鼠的感觉运动皮层某一特定区域缓慢压迫引起的中度脑缺血进行长达9天的行为学和形态学观察。脑缺血后的功能缺陷通过每日束走试验评估,形态学变化分别在第1、2、3、5和9天通过尼氏染色进行验证。暴露于脑缺血的大鼠表现出梁行走能力受损。轻度低温可以防止挤压导致的功能缺陷和脑损伤。年幼(5周)的动物比年长(9周)的动物表现出更少的神经功能缺陷。组织学检查显示,从第1天到第3天,主要受损脑区受损锥体神经元数量明显增加。在第3天至第5天,损伤细胞数量保持不变,此后第9天检测到硫离子阳性神经元缓慢下降。非竞争性NMDA受体拮抗剂二唑西平(MK-801, 3mg /kg, i.p)在第1天没有改变神经损伤,但此后提高了功能恢复的速度,减少了受损细胞的数量。AMPA受体拮抗剂LY326325(15或30 mg/kg; i.p)剂量依赖性地减少了第1天的神经功能缺损,提高了恢复速度,并随着时间的推移减少了损伤神经元的数量。我们的数据表明,对感觉运动皮层中定义明确的大脑区域进行短时硬膜外压迫是一种高度可重复的模型,在研究脑缺血后的功能和形态学后果以及评估新型神经保护药理药物的治疗潜力方面具有很高的成功率。
Behavioral and morphological changes were examined for up to 9 days after moderate cerebral ischemia caused by slow compression of a specific brain area in the sensorimotor cortex of Sprague-Dawley rats. Functional deficits after the cerebral ischemia were assessed by daily beam-walking tests, whereas morphological changes were verified using Nissl staining on day 1, 2, 3, 5, and 9, respectively. Rats exposed to cerebral ischemia displayed impaired beam walking performance. Mild hypothermia prevented both the compression-produced functional deficits and the brain damage. Younger (5 weeks) animals showed less neurological deficits than older (9 weeks) animals. Histological examination revealed a pronounced increase in the number of injured pyramidal neurons from day 1 to day 3 in the primarily damaged brain region. Between day 3 and day 5, the number of injured cells remained constant, whereafter there was a slow decline of thionin-positive neurons as examined on day 9. The noncompetitive NMDA receptor antagonist, dizocilpine (MK-801; 3 mg/kg, i.p.), did not alter the neurological impairment on day 1, but improved thereafter the rate of functional recovery and reduced the number of damaged cells. The AMPA receptor antagonist, LY326325 (15 or 30 mg/kg; i.p.), dose-dependently diminished the neurological deficits on day 1, enhanced the rate of recovery, and reduced the number of injured neurons over time. Our data suggest that short-lasting extradural compression of a well-defined brain area in the sensorimotor cortex is a highly reproducible model with a high success rate for the study of functional and morphological consequences after cerebral ischemia as well as for the evaluation of the therapeutic potential of novel, neuroprotective pharmacological agents.
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