The massive dopaminergic loss in Parkinson’s disease (PD) is accompanied by marked alterations in striatal neuronal plasticity demonstrated in experimental models. In human PD, a severe loss of plasticity of the primary motor cortex (M1) exists from the very early stages of development of motor signs. This was inferred from human experiments using non invasive cortical stimulation techniques (mainly transcranial magnetic stimulation). However, the status of motor cortical plasticity in animal models of PD has not been extensively explored. Even though there is no strong evidence to associate plastic changes in M1 with the clinical signs of PD, these plastic changes in M1 are viewed as the consequence of the same dysfunction in the striato-thalamo-cortical pathway that causes motor signs. Alternatively, the direct effect of dopaminergic deficiency or excess during treatment and the molecular consequences thereof at M1 or of the effect of alterations in other networks secondarily impacted by striato-cortical dysfunction, could affect M1 plasticity. The contribution of the mesocortical system or the cerebello-thalamo-cortical system to changes in M1 plasticity or motor learning in PD are not yet fully unravelled.
During the course of PD, the response of M1plasticity to dopaminergic replacement shows dynamic changes. This raises the important questions of whether such changes are behaviourally significant or are mere epiphenomena arising from alterations upstream in the levels of dopamine, due to disease or as a consequence of non physiological dopamine replacement therapy. More specifically, we can debate whether impaired motor cortical plasticity influences the occurrence of motor complications like dyskinesias or impacts higher level motor functions like motor learning and programming. It is still unknown whether motor learning undergoes dynamic changes akin to the motor response fluctuations in the motor signs of PD that are attributed to the loss of long duration response to dopaminergic treatment. Innumerable imaging studies using the most recent sophisticated techniques have been conducted in PD. Yet they have hardly contributed to dissociating between behaviourally relevant changes and epiphenomena in neural networks.
Review articles and original research using animal or human models that explore the mechanisms and perspectives of motor cortex plasticity and its link to motor learning and dopamine deficiency in PD and the role of extra striatal networks can be proposed. We aim at providing an updated review that will facilitate discussions about this topic across scientific disciplines.
The massive dopaminergic loss in Parkinson’s disease (PD) is accompanied by marked alterations in striatal neuronal plasticity demonstrated in experimental models. In human PD, a severe loss of plasticity of the primary motor cortex (M1) exists from the very early stages of development of motor signs. This was inferred from human experiments using non invasive cortical stimulation techniques (mainly transcranial magnetic stimulation). However, the status of motor cortical plasticity in animal models of PD has not been extensively explored. Even though there is no strong evidence to associate plastic changes in M1 with the clinical signs of PD, these plastic changes in M1 are viewed as the consequence of the same dysfunction in the striato-thalamo-cortical pathway that causes motor signs. Alternatively, the direct effect of dopaminergic deficiency or excess during treatment and the molecular consequences thereof at M1 or of the effect of alterations in other networks secondarily impacted by striato-cortical dysfunction, could affect M1 plasticity. The contribution of the mesocortical system or the cerebello-thalamo-cortical system to changes in M1 plasticity or motor learning in PD are not yet fully unravelled.
During the course of PD, the response of M1plasticity to dopaminergic replacement shows dynamic changes. This raises the important questions of whether such changes are behaviourally significant or are mere epiphenomena arising from alterations upstream in the levels of dopamine, due to disease or as a consequence of non physiological dopamine replacement therapy. More specifically, we can debate whether impaired motor cortical plasticity influences the occurrence of motor complications like dyskinesias or impacts higher level motor functions like motor learning and programming. It is still unknown whether motor learning undergoes dynamic changes akin to the motor response fluctuations in the motor signs of PD that are attributed to the loss of long duration response to dopaminergic treatment. Innumerable imaging studies using the most recent sophisticated techniques have been conducted in PD. Yet they have hardly contributed to dissociating between behaviourally relevant changes and epiphenomena in neural networks.
Review articles and original research using animal or human models that explore the mechanisms and perspectives of motor cortex plasticity and its link to motor learning and dopamine deficiency in PD and the role of extra striatal networks can be proposed. We aim at providing an updated review that will facilitate discussions about this topic across scientific disciplines.
