Nucleus reticularis tegmenti pontis: a bridge between the basal ganglia and cerebellum for movement control.

Nucleus reticularis tegmenti pontis: a bridge between the basal ganglia and cerebellum for movement control.
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脑桥被盖网状核:基底节与小脑之间的运动控制桥梁。

DOI:
10.1007/s00221-023-06574-0
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发表时间:
2023-05
影响因子:
2
通讯作者:
Pong, Milton
Pong, Milton
中科院分区:
医学4区
文献类型:
--
作者:
Gibson, Alan R.;Horn, Kris M.;Pong, Milton

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基底神经节中的神经处理对于正常运动至关重要。基底神经节疾病,如帕金森病,产生各种运动障碍,包括运动不能和运动迟缓。许多人认为,基底神经节通过丘脑投射到大脑皮层的运动区和投射到小脑来影响运动,小脑也通过丘脑投射到运动皮层。然而,中断这些丘脑到皮质的通路的病变对许多运动(包括肢体运动)几乎没有影响。然而,肢体运动严重受损的基底神经节疾病或损害小脑。如果基底神经节和小脑的输出不经过丘脑而到达脑干运动区,我们就可以解释这种损害以及丘脑病变的轻微影响。在这份报告中,我们描述了几个脑干通路,连接基底神经节输出到小脑通过脑桥被盖网状核(NRTP)。此外,我们提出广泛的传入和传出连接的NRTP与小脑可以整合处理小脑区域。然后,基底神经节可以通过小脑的下行投射来改变运动。通过NRTP的途径对于正常运动的控制是重要的,并且可能是与基底神经节疾病相关的缺陷的基础。
Neural processing in the basal ganglia is critical for normal movement. Diseases of the basal ganglia, such as Parkinson’s disease, produce a variety of movement disorders including akinesia and bradykinesia. Many believe that the basal ganglia influence movement via thalamic projections to motor areas of the cerebral cortex and through projections to the cerebellum, which also projects to the motor cortex via the thalamus. However, lesions that interrupt these thalamic pathways to the cortex have little effect on many movements, including limb movements. Yet, limb movements are severely impaired by basal ganglia disease or damage to the cerebellum. We can explain this impairment as well as the mild effects of thalamic lesions if basal ganglia and cerebellar output reach brainstem motor regions without passing through the thalamus. In this report, we describe several brainstem pathways that connect basal ganglia output to the cerebellum via nucleus reticularis tegmenti pontis (NRTP). Additionally, we propose that widespread afferent and efferent connections of NRTP with the cerebellum could integrate processing across cerebellar regions. The basal ganglia could then alter movements via descending projections of the cerebellum. Pathways through NRTP are important for the control of normal movement and may underlie deficits associated with basal ganglia disease.
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