Bio

Dr. Chattree is a board-certified neurologist with the Stanford Movement Disorders Center and an Instructor in the Department of Neurology and Neurological Sciences. He provides comprehensive care for patients with movement disorders, which includes deep brain stimulation evaluation/programming and botulinum toxin injections. In addition to his clinical practice, Dr. Chattree conducts research in the lab of Dr. Mark Schnitzer at Stanford, where he uses optical and genetic techniques in mice to develop new treatments for movement disorders.

Clinical Focus

  • Neurology
  • Movement Disorders
  • Parkinson's Disease

Academic Appointments

Professional Education

  • Fellowship: Stanford University Behavioral Neurology Fellowship (2023) CA
  • Board Certification: American Board of Psychiatry and Neurology, Neurology (2021)
  • Residency: Stanford University Dept of Neurology (2021) CA
  • Internship: Stanford University Internal Medicine Residency (2018) CA
  • Medical Education: University of Texas Southwestern Medical School (2017) TX

Contact

  • Academic
    gchatt@stanford.edu
    University - Other Teaching/Research Department: Adult Neurology Position: Instructor
  • Clinical (Primary)  Stanford Neuroscience Health Center 213 Quarry Rd MC 5957 Fl 2 Palo Alto, CA 94304 (650) 721-4797 (fax)

Additional Clinical Info

Additional Info

  • Mail Code: 5327

All Publications

  • Video Teaching NeuroImages: Atypical abnormal eye movements in PNPO-related Epilepsy. Neurology Pavitt, S., Karamian, A. G., Chattree, G., Klotz, J., Beres, S. 2020

    View details for DOI 10.1212/WNL.0000000000010861

    View details for PubMedID 32913027

  • A Basal Ganglia Circuit Sufficient to Guide Birdsong Learning. Neuron Xiao, L., Chattree, G., Oscos, F. G., Cao, M., Wanat, M. J., Roberts, T. F. 2018; 98 (1): 208-221.e5

    Abstract

    Learning vocal behaviors, like speech and birdsong, is thought to rely on continued performance evaluation. Whether candidate performance evaluation circuits in the brain are sufficient to guide vocal learning is not known. Here, we test the sufficiency of VTA projections to the vocal basal ganglia in singing zebra finches, a songbird species that learns to produce a complex and stereotyped multi-syllabic courtship song during development. We optogenetically manipulate VTA axon terminals in singing birds contingent on how the pitch of an individual song syllable is naturally performed. We find that optical inhibition and excitation of VTA terminals are each sufficient to reliably guide learned changes in song. Inhibition and excitation have opponent effects on future performances of targeted song syllables, consistent with positive and negative reinforcement of performance outcomes. These findings define a central role for reinforcement mechanisms in learning vocalizations and demonstrate minimal circuit elements for learning vocal behaviors. VIDEO ABSTRACT.

    View details for DOI 10.1016/j.neuron.2018.02.020

    View details for PubMedID 29551492

    View details for PubMedCentralID PMC5918681

  • Identification of a motor-to-auditory pathway important for vocal learning. Nature neuroscience Roberts, T. F., Hisey, E., Tanaka, M., Kearney, M. G., Chattree, G., Yang, C. F., Shah, N. M., Mooney, R. 2017

    Abstract

    Learning to vocalize depends on the ability to adaptively modify the temporal and spectral features of vocal elements. Neurons that convey motor-related signals to the auditory system are theorized to facilitate vocal learning, but the identity and function of such neurons remain unknown. Here we identify a previously unknown neuron type in the songbird brain that transmits vocal motor signals to the auditory cortex. Genetically ablating these neurons in juveniles disrupted their ability to imitate features of an adult tutor's song. Ablating these neurons in adults had little effect on previously learned songs but interfered with their ability to adaptively modify the duration of vocal elements and largely prevented the degradation of songs' temporal features that is normally caused by deafening. These findings identify a motor to auditory circuit essential to vocal imitation and to the adaptive modification of vocal timing.

    View details for DOI 10.1038/nn.4563

    View details for PubMedID 28504672