| Literature DB >> 28858620 |
Jeongjin Kim1, Youngsoo Kim2, Ryuichi Nakajima3, Anna Shin4, Minju Jeong4, Ah Hyung Park4, Yongcheol Jeong4, Seonmi Jo4, Seungkyoung Yang4, Hosung Park5, Sung-Hwan Cho6, Kwang-Hyun Cho6, Insop Shim7, Jae Hoon Chung4, Se-Bum Paik6, George J Augustine8, Daesoo Kim9.
Abstract
Basal ganglia (BG) circuits orchestrate complex motor behaviors predominantly via inhibitory synaptic outputs. Although these inhibitory BG outputs are known to reduce the excitability of postsynaptic target neurons, precisely how this change impairs motor performance remains poorly understood. Here, we show that optogenetic photostimulation of inhibitory BG inputs from the globus pallidus induces a surge of action potentials in the ventrolateral thalamic (VL) neurons and muscle contractions during the post-inhibitory period. Reduction of the neuronal population with this post-inhibitory rebound firing by knockout of T-type Ca2+ channels or photoinhibition abolishes multiple motor responses induced by the inhibitory BG input. In a low dopamine state, the number of VL neurons showing post-inhibitory firing increases, while reducing the number of active VL neurons via photoinhibition of BG input, effectively prevents Parkinson disease (PD)-like motor symptoms. Thus, BG inhibitory input generates excitatory motor signals in the thalamus and, in excess, promotes PD-like motor abnormalities. VIDEO ABSTRACT.Entities:
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Year: 2017 PMID: 28858620 DOI: 10.1016/j.neuron.2017.08.028
Source DB: PubMed Journal: Neuron ISSN: 0896-6273 Impact factor: 17.173