Subcortical middle cerebral artery ischemia abolishes the digit flexion and closing used for grasping in rat skilled reaching

被引:35
作者
Gharbawie, OA
Auer, RN
Whishaw, IQ
机构
[1] Univ Lethbridge, Canadian Ctr Behav Neurosci, Dept Psychol & Neurosci, Lethbridge, AB T1K 3M4, Canada
[2] Univ Calgary, Dept Pathol & Clin Neurosci, Calgary, AB T2N 4N1, Canada
基金
加拿大自然科学与工程研究理事会;
关键词
grasping; middle cerebral artery; transient ischemia; skilled reaching; basal ganglia; digits;
D O I
10.1016/j.neuroscience.2005.10.043
中图分类号
Q189 [神经科学];
学科分类号
071006 [神经生物学];
摘要
That rats reach for and grasp a food item using a single paw has prompted their use in neurobiological studies of skilled movements and modeling neural injury including middle cerebral artery stroke. Although motor system lesions have been shown to disrupt various qualitative aspects of the transport of a limb to a food target and withdrawal of the limb with the food, no lesion has been found to abolish digit flexion for grasping. Here, rats received unilateral transient middle cerebral artery ischemia that was restricted mainly to subcortical tissue of the forebrain (caudate-putamen, globus pallidus, and associated fibers) or a sham operation. Both paws were later trained and evaluated on skilled reaching using a rating scale for digit use. Middle cerebral artery rats did not flex and close their digits to grasp food when using their contralateral-to-lesion limb. The grasp impairment was not due to a failure to learn the task as middle cerebral artery rats used the ipsilateral limb as successfully as control rats and they were reinforced for reaching by raking food into the reaching box using an open paw. The impairment was also not due to an inability to move the digits, as they were flexed and closed in other phases of the reach. The paradigm should prove useful for further studies of rehabilitation in relation to the idea that digit closure may be controlled by the joint action of a number of neural systems that converge in the basal ganglia. (c) 2005 IRBO. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:1107 / 1118
页数:12
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