Clinical Focus

  • Anesthesia

Academic Appointments

Honors & Awards

  • Internal Grant Program Award, Department of Anesthesiology, Pain & Perioperative Medicine (2012)
  • Oustanding Contributions to Anesthesia Research, Department of Anesthesiology, Pain & Perioperative Medicine (2013)
  • Mentored Research Training Grant - Basic Science, Foundation for Anesthesia Education and Research (2013-2015)

Professional Education

  • Board Certification: Anesthesia, American Board of Anesthesiology (2014)
  • Residency:Stanford University School of Medicine (2013) CA
  • Internship:Memorial Sloan-Kettering Cancer Center (2010) NY
  • Fellowship, Stanford Hospital & Clinics, Research (2013)
  • Medical Education:Albert Einstein College of Medicine (2009) NY
  • PhD, Albert Einstein College of Medicine, Neuroscience (2009)
  • BS, Yale University, Psychobiology/Neuroscience (1999)

Research & Scholarship

Current Research and Scholarly Interests

Neurosurgery for intractable neuropsychiatric illness has emerged as a safe and effective treatment option for many patients, most notably those with Parkinson’s Disease (PD). Deep Brain Stimulation (DBS) reduces PD patients’ symptoms and drug-related side effects. Advances in the nascent field of optogenetics have led to the discovery of a neural circuit crucial for producing the therapeutic response to DBS, centered on cortical afferents to the subthalamic nucleus (STN). We hypothesize that selective, long lasting modification of synapses within this circuit will improve efficacy of DBS. We describe a method to selectively study the synapses of neural pathways underlying DBS’ therapeutic effect, using transgenic mice whose PD-like symptoms are reversed by optical stimulation. We are currently developing neuroactive compounds that could be developed as intraoperative therapeutic adjuncts to existing or modified DBS protocols.


All Publications

  • Decreased motivation during chronic pain requires long-term depression in the nucleus accumbens SCIENCE Schwartz, N., Temkin, P., Jurado, S., Lim, B. K., Heifets, B. D., Polepalli, J. S., Malenka, R. C. 2014; 345 (6196): 535-542


    Several symptoms associated with chronic pain, including fatigue and depression, are characterized by reduced motivation to initiate or complete goal-directed tasks. However, it is unknown whether maladaptive modifications in neural circuits that regulate motivation occur during chronic pain. Here, we demonstrate that the decreased motivation elicited in mice by two different models of chronic pain requires a galanin receptor 1-triggered depression of excitatory synaptic transmission in indirect pathway nucleus accumbens medium spiny neurons. These results demonstrate a previously unknown pathological adaption in a key node of motivational neural circuitry that is required for one of the major sequela of chronic pain states and syndromes.

    View details for DOI 10.1126/science.1253994

    View details for Web of Science ID 000339651300039

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