Motor cortical activities in the animal model of Parkinson's disease
Other conference paper


摘要The primary motor cortex (M1) is responsible for motor execution and contributes to acquisition of new motor skills. Previous studies show that M1 layer V pyramidal neurons have increased burst firing and increased beta power in Parkinson's disease (PD) model. However, most studies have focused on recording extracellular activity in vivo or intracellular properties in vitro in M1. Properties of these neurons in intact subjects, like the in vivo intrinsic membrane excitability and synaptic inputs, which are important in understanding neuronal integration leading to their outputs, are less well addressed. We therefore applied in vivo whole-cell patch-clamp technique to record from neurons in M1, focusing on layer V. As a first step, we characterized the electrophysiological properties of these neurons in normal mature mice and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice under anesthesia. Neurons were approached, patched blindly and recorded for at least 20 mins. The depth of the neurons was recorded and confirmed by post-mortem biocytin avidin-biotinylated complex method that also revealed the neuronal morphology. Our data show that the intrinsic properties of the neurons, including the resting membrane potential, input resistance and membrane time constant, remain largely unchanged in MPTP-treated mice. Also, the averaged firing rates were unaffected. However, there is an increase in the number of spikes per burst and also a decrease in inter-burst intervals. The proportion of bursty neurons is also increased in MPTP mice. Subthreshold excitatory postsynaptic current (EPSC) and inhibitory postsynaptic current (IPSC) could also be recorded, which could provide insight into the mechanisms underlying changes in the firing patterns in M1 neurons observed in PD subjects.
著者Y. LI, C. LI, Y. GU, W.H. YUNG, Y. KE
會議名稱Neuroscience 2017 (Society for Neuroscience Annual meeting 2017)
會議地點Washington DC

上次更新時間 2018-30-04 於 11:19