Cerebellar influence on motor cortex plasticity: behavioral implications for Parkinson’s disease

Frontiers in Neurology

Sabine eMeunier¹  Traian ePopa²  Asha eKishore³ 

[1] Institut du Cerveau et de la Moelle epiniere (ICM), INSERM U1127, CNRS UMR 7225, Université Pierre et Marie Curie – Paris 6 UMR_S975;Institut du Cerveau et de la Moelle epiniere (ICM);Sree Chitra Tirunal Institute for Medical Sciences and Technology (SCTIMST);

关键词: Basal Ganglia;    Cerebellum;    Dopamine;    Parkinson Disease;    motor cortex plasticity;   

DOI  :  10.3389/fneur.2014.00068

来源: DOAJ

【 摘 要 】

Normal motor behavior involves the creation of appropriate activity patterns across motor networks, enabling firing synchrony, synaptic integration and normal functioning of these net works. Strong topography-specific connections among the basal ganglia, cerebellum and their projections to overlapping areas in the motor cortices suggest that these networks could influence each other’s plastic responses and functions. The defective striatal signaling in Parkinson’s disease (PD) could therefore lead to abnormal oscillatory activity and aberrant plasticity at multiple levels within the interlinked motor networks. Normal striatal dopaminergic signaling and cerebellar sensory processing functions influence the scaling and topographic specificity of M1 plasticity. Both these functions are abnormal in PD and appear to contribute to the abnormal M1 plasticity. Defective motor map plasticity and topographic specificity within M1 could lead to incorrect muscle synergies, which could manifest as abnormal or undesired movements, and as abnormal motor learning in PD. We propose that the loss of M1 plasticity in PD reflects a loss of co-ordination among the basal ganglia, cerebellar and cortical inputs which translates to an abnormal plasticity of motor maps within M1 and eventually to some of the motor signs of PD. The initial benefits of dopamine replacement therapy on M1 plasticity and motor signs are lost during the progressive course of disease. Levodopa-induced dyskinesias in patients with advanced PD is linked to a loss of M1 sensorimotor plasticity and the attenuation of dyskinesias by cerebellar inhibitory stimulation is associated with restoration of M1 plasticity. Complimentary interventions should target reestablishing physiological communication between the striatal and cerebellar circuits, and within striato-cerebellar loop. This may facilitate correct motor synergies and reduce abnormal movements in PD.

【 授权许可】

Unknown