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Effects of reducing sensory-motor feedback on the appearance of crossed nigro-thalamic projections and recovery from turning induced by unilateral substantia nigra lesions.

作者信息

Morgan S, Huston J P, Pritzel M

出版信息

Brain Res Bull. 1983 Dec;11(6):721-7. doi: 10.1016/0361-9230(83)90014-x.

Abstract

This experiment addressed the question of whether the increase in interhemispheric nigrothalamic projections, found after unilateral lesions of the substantia nigra (SN), is related to recovery from the lesion-induced sensory-motor asymmetry. We examined the effects of diminished information feedback about the animals' own behavior on recovery from turning induced by unilateral substantia nigra lesions, and the appearance of an increase in number of crossed nigro-thalamic projections. The animals received unilateral 6-hydroxydopamine lesions and were placed in a hammock for the next 7 days. Thus, they were prevented from engaging in turning behavior. They were then implanted with horseradish peroxidase (HRP) in the thalamus ipsilateral to the lesion. No HRP-labeled cells were found in the SN contralateral to the HRP implantation in these animals. In rats, which were allowed 7 days normal interaction with the environment subsequent to unilateral SN damage, labeled cells were found in the undamaged SN when HRP was implanted in the thalamus ipsilateral to the lesion. Animals which were kept in the hammock and subsequently allowed a week of normal interaction with the environment showed the same pattern of recovery from turning behavior as the animals which were allowed to recover normally immediately after the unilateral SN lesion. It was concluded that the relationship between the appearance of the nigro-thalamic projections and the cessation of turning behavior is not fortuitous. Also, it would appear that some form of sensory-motor learning is involved in the recovery of function after unilateral SN lesions. Thus, the results substantiate the idea that these cross-projections form part of a physical basis of recovery from unilateral lesion-induced asymmetries.

摘要

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