LOCOMOTOR AND PASSIVE-AVOIDANCE DEFICITS FOLLOWING OCCLUSION OF THE MIDDLE CEREBRAL-ARTERY
LOCOMOTOR AND PASSIVE-AVOIDANCE DEFICITS FOLLOWING OCCLUSION OF THE MIDDLE CEREBRAL-ARTERY
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DOI：
10.1016/0031-9384(95)00103-p
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发表时间：
1995-11-01
影响因子：
2.9
通讯作者：
SANBERG, PR
中科院分区：
文献类型：
--
作者：
BORLONGAN, CV;CAHILL, DW;SANBERG, PR
大脑中动脉（MCA）闭塞后感觉、运动和认知功能障碍的表征是在缺血动物模型中研究治疗干预的先决条件。使用不同的策略来诱导缺血，但据报道，MCA的局灶性短暂闭塞导致的神经病理学与临床脑缺血中所见的最相似。如果MCA闭塞技术导致中风动物模型，那么中风中固有的行为障碍应该在该模型中表现出来。本研究提供了与MCA闭塞相关的行为改变的进一步表征。Sprague-Dawley大鼠右侧MCA暂时闭塞，在缺血后1个月和2个月，随后测试了被动回避行为、运动协调、不对称运动行为、神经功能、夜间自发和苯丙胺诱导的运动活动以及氟哌啶醇诱导的僵住症。结果表明，缺血大鼠表现出长期的感觉，运动和认知功能的损害。与其他报告时间MCA诱导的行为缺陷的研究的差异可能是由于用于诱导缺血和随后的CNS损伤的技术，测试时间段的差异（即，即刻与稍后的缺血后，夜间与白天），实验过程中的测试-再测试次数，以及动物的年龄。MCA诱导的行为变化所涉及的机制可能是纹状体神经元上多巴胺受体的丧失。组织学分析显示损伤仅限于纹状体的侧面。这些行为和解剖学数据支持MCA闭塞作为缺血模型，并阐明了在表征MCA诱导的神经病理学改变时应控制的重要因素。
The characterization of sensory, motor and cognitive dysfunctions following occlusion of the middle cerebral artery (MCA) is prerequisite to investigations of treatment intervention in animal models of ischemia. Different strategies are used to induce ischemia, but the focal, transient occlusion of the MCA has been reported to result in neuropathology most similar to that seen in clinical cerebral ischemia. If the MCA occlusion technique results in a stroke animal model, then the behavioral impairments inherent in stroke should be manifested in this model. The present study provides a further characterization of behavioral alterations associated with MCA occlusion. Sprague-Dawley rats underwent temporal occlusion of the right MCA, and at 1 mo and 2 mo postischemia, were subsequently tested in passive avoidance behavior, motor coordination, asymmetrical motor behavior, neurological functioning, nocturnal spontaneous and amphetamine-induced locomotor activity, and haloperidol-induced catalepsy. Results revealed that ischemic rats showed long-term impairments in sensory, motor and cognitive functions. The discrepancy with other studies reporting temporal MCA-induced behavioral deficits may be due to techniques used to induce ischemia and consequent CNS damage, differences in time period of testing (i.e., immediate vs. later postischemia, nighttime vs. daytime), number of test-retests over the course of the experiment, and age of the animals. The mechanism involved in the MCA-induced behavioral changes may be represented by loss of dopamine receptors on striatal neurons. Histological analysis revealed damage limited to the lateral aspect of the striatum. These behavioral and anatomical data support MCA occlusion as a model of ischemia, and elucidate important factors that should be controlled for in characterizing the MCA-induced neuropathological alterations.