Dopamine depletion selectively disrupts interactions between striatal neuron subtypes and LFP oscillations

Dana Zemel, Howard Gritton, Cyrus Cheung, Sneha Shankar, Mark Kramer, Xue Han

Research output: Contribution to journalArticlepeer-review


Dopamine degeneration in Parkinson's disease (PD) dysregulates the striatal neural network and causes motor deficits. However, it is unclear how altered striatal circuits relate to dopamine-acetylcholine chemical imbalance and abnormal local field potential (LFP) oscillations observed in PD. We perform a multimodal analysis of the dorsal striatum using cell-type-specific calcium imaging and LFP recording. We reveal that dopamine depletion selectively enhances LFP beta oscillations during impaired locomotion, supporting beta oscillations as a biomarker for PD. We further demonstrate that dynamic cholinergic interneuron activity during locomotion remains unaltered, even though cholinergic tone is implicated in PD. Instead, dysfunctional striatal output arises from elevated coordination within striatal output neurons, which is accompanied by reduced locomotor encoding of parvalbumin interneurons and transient pathological LFP high-gamma oscillations. These results identify a pathological striatal circuit state following dopamine depletion where distinct striatal neuron subtypes are selectively coordinated with LFP oscillations during locomotion.

Original languageEnglish (US)
Article number110265
JournalCell Reports
Issue number3
StatePublished - Jan 18 2022
Externally publishedYes


  • Parkinson's disease
  • basal ganglia
  • beta oscillations
  • gamma oscillations
  • immobility
  • local field potential
  • population dynamics
  • striatum

ASJC Scopus subject areas

  • General Biochemistry, Genetics and Molecular Biology


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