Impaired synaptic plasticity in the primary motor cortex and motor skill consolidation after dopamine depletion

37th Congress of IUPS (Birmingham, UK) (2013) Proc 37th IUPS, PCC121

Poster Communications: Impaired synaptic plasticity in the primary motor cortex and motor skill consolidation after dopamine depletion

Q. Li1,2, Y. Ke1,2, W. Yung1,2

1. School of Biomedical Sciences, Faculty of Medicine, the Chinese University of Hong Kong, New Territories, Hong Kong. 2. Shenzhen Research Institute, the Chinese University of Hong Kong, Shen Zhen, Guang Dong, China.

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The ability to learn and retain new motor skills is important in daily life. After repeated exposure to a specific procedure, motor skill becomes more accurate and automatic. In Parkinson’s disease (PD), in spite of the cardinal motor symptoms like akinesia and bradykinesia, patients suffer deficits in motor skill learning. The impaired synaptic plasticity of basal ganglia circuitry has been suggested to be involved. In PD, dopamine innervation originating from the mesocortical pathway is reduced in the primary motor cortex (MI), an area that also contributes to motor learning. However, the impact of dopamine depletion on cortical synaptic plasticity and motor skill learning is not clear. The present study addresses these questions based on in vivo long-term potentiation (LTP) in the MI and motor training on PD rats. 6-hydroxydopamine was bilaterally injected into the MI (AP: +2.5, ML: ±3.0, DV: 1.7mm) of SD rats. After one week’s recovery, arm-reaching for food task was conducted (10 trials) to confirm the preferred forelimb being used. A 16-channel microwire recording electrode and a bipolar stimulus electrode (300µm apart) were implanted into contralateral MI forelimb territory, targeting at layer V. In the first set of experiments, intermittent high frequency stimulation (iHFS, 90 trains delivered every 10s; each train consisted of 50 pulses in 250Hz) was delivered to the MI of freely moving rats and evoked local field potential (LFP) was monitored. In the sham-operated group, LTP level was measured as the increment of evoked LFP amplitude 90 mins after the induction protocol (132.8±3.1%, n=4). In contrast, the cortical LTP in the 6-OHDA group was significantly reduced (110.8±3.0%, n=3, **p<0.01, compared with sham). In the second set of experiments, arm-reaching task was performed to investigate the correlation between cortical LTP impairment and performance of motor skill. The skillfulness was assessed by the rate of ‘single success’, namely food pellet obtained on the first reaching attempt. The performance of the PD rats in the initial learning phase was comparable to that of the sham-operated group (1st day: sham, 32.4±1.1%, n=3; 6-OHDA lesion, 30.2±1.8%, n=3; p=0.36). As training continued, PD animals exhibited deficit in consolidating the motor skill, even if they could reach a good success rate in the previous day. After 1 week’s training, a significant difference in the ‘single success’ rate between the two groups was found (sham: 45.1±2.8%, n=3; 6-OHDA lesion: 30.9±4.1%, n=3; *p<0.05). Our study showed that dopamine depletion confined to the MI could lead to impairment in cortical LTP which may preferentially affect the consolidation, but not the acquisition of motor skills.



Where applicable, experiments conform with Society ethical requirements.

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