Qiaoling Cui

Microglial sTREM2 limits dyskinesia and acts on TrkB to support circuit plasticity

The paper identifies a microglial gene program linked to dyskinesia in Parkinson's disease and shows that sTREM2 reduces dyskinesia by modulating TrkB signaling and synaptic plasticity.

Cell- and state-specific plasticity of striatal glutamatergic synapses is critical to the expression of levodopa-induced dyskinesia

This study identifies GluN2B-containing NMDAR up-regulation in iSPNs as a key mechanism in LID, showing that targeting these receptors can reduce dyskinesia without affecting levodopa's motor benefits.

State-dependent modulation of spiny projection neurons controls levodopa-induced dyskinesia in a mouse model of Parkinson's disease

This study identifies state-dependent modulation of spiny projection neurons in a mouse Parkinson's model and shows how disrupting specific signaling pathways reduces levodopa-induced dyskinesia.

Dissociable Roles of Pallidal Neuron Subtypes in Regulating Motor Patterns

This study identifies distinct GPe neuron subtypes using mouse lines and shows their unique roles in motor behavior and anxiety-like behavior through optogenetics and machine learning.

Striatal Direct Pathway Targets Npas1+ Pallidal Neurons

This study identifies that direct-pathway striatal projection neurons (dSPNs) target Npas1+ neurons in the external globus pallidus (GPe) and show that this projection suppresses movement, contributing to Parkinson's disease hypokinesia.

Parvalbumin+ and Npas1+ Pallidal Neurons Have Distinct Circuit Topology and Function

This study identifies distinct roles of PV+ and Npas1+ neurons in the GPe for locomotion and shows differences in their synaptic inputs from the STN in Parkinson's disease.

Npas1+-Nkx2.1+ Neurons Form A Unique Pallidal Neuron Subclass

The paper identifies Npas1+-Nkx2.1+ neurons as a distinct subclass of GPe neurons and describes their role in the cortico-pallido-cortical loop.