Abstract:
:The motor symptoms of Parkinson's disease (PD) are thought to stem from an imbalance in the activity of striatal direct- and indirect-pathway spiny projection neurons (SPNs). Disease-induced alterations in the activity of networks controlling SPNs could contribute to this imbalance. One of these networks is anchored by the parafascicular nucleus (PFn) of the thalamus. To determine the role of the PFn in striatal PD pathophysiology, optogenetic, chemogenetic, and electrophysiological tools were used in ex vivo slices from transgenic mice with region-specific Cre recombinase expression. These studies revealed that in parkinsonian mice, the functional connectivity of PFn neurons with indirect pathway SPNs (iSPNs) was selectively enhanced by cholinergic interneurons acting through presynaptic nicotinic acetylcholine receptors (nAChRs) on PFn terminals. Attenuating this network adaptation by chemogenetic or genetic strategies alleviated motor-learning deficits in parkinsonian mice, pointing to a potential new therapeutic strategy for PD patients.
journal_name
Neuronjournal_title
Neuronauthors
Tanimura A,Du Y,Kondapalli J,Wokosin DL,Surmeier DJdoi
10.1016/j.neuron.2018.12.004subject
Has Abstractpub_date
2019-02-06 00:00:00pages
444-458.e6issue
3eissn
0896-6273issn
1097-4199pii
S0896-6273(18)31080-8journal_volume
101pub_type
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