Anatol Kreitzer, PhD
Senior Investigator, Gladstone Institute of Neurological Disease

Other Professional Titles

Professor, Physiology and Neurology, University of California, San Francisco


(415) 734-2507


(415) 355-0824


Erica Delin
(415) 734-2516

Areas of Investigation

The Kreitzer laboratory has made important advances in understanding the brain circuitry that goes awry in Parkinson’s disease and dyskinesia. Using a technique called optogenetics, the lab established how activating specific types of cells in the basal ganglia could either mimic or reverse symptoms of Parkinson’s disease.  Kreitzer’s group further mapped how this circuitry can influence walking, through connections with a part of the brain called the mesencephalic locomotor region. Using high-resolution recording techniques, the lab also identified specific biochemical signaling pathways in these cells that are altered in mouse models of Parkinson’s disease and dyskinesia, and identified how changes in the structure and activity of these cells can lead to unwanted decreases or increases in movement. The Kreitzer laboratory is also beginning to delve into how this same circuitry is implicated in neuropsychiatric diseases such as obsessive-compulsive disorder (OCD), Tourette syndrome, and attention deficit and hyperactivity disorder (ADHD), with the aim of identifying specific cell types and circuits that underlie deficits in behavioral switching, repetitive behaviors, tics, and hyperactivity.

Lab Focus

What is the functional role of neural activity in direct and indirect pathway medium-spiny neurons (MSNs) found in the basal ganglia?
How do striatal microcircuits function to shape direct and indirect pathway output?
What role does dopamine play in striatal microcircuit function?
How does loss of dopamine impact basal ganglia circuit function?
How do dopamine and other neuromodulators modulate synaptic plasticity in the striatum?
How can we restore basal ganglia circuit function in the absence of dopamine, such as during PD?


Developed the capability to directly activate basal ganglia circuitry in vivo, using optogenetic control of direct- and indirect-pathway MSNs.
Established a critical role for basal ganglia circuitry in the bidirectional regulation of motor behavior and reinforcement learning.
Identified novel therapeutic targets for the amelioration of parkinsonian symptoms.


  • Society for Neuroscience
  • International Basal Ganglia Society

Professional titles

Professor, Physiology and Neurology, University of California, San Francisco


  • University of California, Berkeley
  • Harvard University

Honors and Awards

2011 IACM Award for Young Researchers
2011 Young Investigator Award, Society for Neuroscience
2010 McKnight Scholar Award
2008 Pew Scholar in Biomedical Sciences