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In vivo electrophysiology of nigral and thalamic neurons in alpha-synuclein over-expressing mice highlights differences from toxin-based models of parkinsonism.
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J Neurophysiol 2013 Sep;
Authors: Collin J Lobb, Abdul K Zaheer, Yoland Smith, Dieter Jaeger
Numerous studies have suggested that alpha-synuclein plays a prominent role in both familial and idiopathic Parkinson's disease (PD). Mice in which human alpha-synuclein are over-expressed (ASO) display progressive motor deficits and many non-motor features of PD. However, it is unclear what in vivo pathophysiological mechanisms drive these motor deficits. It is also unknown whether previously proposed pathophysiological features (i.e. increased beta oscillations, bursting and synchronization) described in toxin-based, nigrostriatal dopamine-depletion models are also present in ASO mice. To address these issues, we first confirmed that 5-6 months old ASO mice have robust motor dysfunction, despite no significant nigrostriatal dopamine degeneration. In the same animals, we then recorded simultaneous single-units and local field potentials (LFP) in the substantia nigra pars reticulata (SNpr), the main basal ganglia output nucleus, and one of its main thalamic targets, the ventromedial nucleus, as well as LFPs in the primary motor cortex in anesthetized ASO mice and their age-matched, wild-type littermates. Neural activity was examined during slow wave activity and desynchronized cortical states, as previously described in 6-hydroxydopamine-lesioned rats. In contrast to toxin-based models, we found a small decrease, rather than an increase, in beta oscillations in the desynchronized state. Similarly, synchronized burst firing of nigral neurons observed in toxin-based models was not observed in ASO mice. Instead, we found more subtle changes in pauses of SNpr firing compared to wild-type controls. Our results suggest that the pathophysiology underlying motor dysfunction in ASO mice is distinctly different from striatal dopamine depletion models of parkinsonism.
PMID: 24068758 [PubMed - as supplied by publisher]