Bio

Bio


Dr. Boris Heifets, MD, PhD, is a board certified anesthesiologist who specializes in providing anesthesia for neurological surgery. He has practiced at Stanford since 2010.

After completing residency training at Stanford, Dr. Heifets completed fellowship training in neuroanesthesiology, also at Stanford. In addition to treating patients, Dr. Heifets also spends a significant amount of time in the lab, where he is investigating the ways in which psychiatric therapies change the function of neural circuits and synapses in the brain.

Dr. Heifets has a special interest in neural stimulation-based treatments for psychiatric and neurological disorders.

Clinical Focus


  • Anesthesia
  • Neuroanesthesia

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


  • Fellowship:Stanford University Dept of Anesthesiology (2016) CA
  • 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


Harnessing synaptic plasticity to treat neuropsychiatric disease

Publications

All Publications


  • MDMA as a Probe and Treatment for Social Behaviors. Cell Heifets, B. D., Malenka, R. C. 2016; 166 (2): 269-72

    Abstract

    MDMA, better known as the recreational drug "ecstasy," is well known for stimulating a feeling of closeness and empathy in its users. We advocate that exploring its mechanism of action could lead to new treatments for psychiatric conditions characterized by impairments in social behavior.

    View details for DOI 10.1016/j.cell.2016.06.045

    View details for PubMedID 27419864

  • Chronic pain. 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

    Abstract

    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 PubMedID 25082697

  • 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
  • Acute Cardiovascular Toxicity of Low-Dose Intrathecal Ziconotide. Pain medicine (Malden, Mass.) Heifets, B. D., Smith, S. M., Leong, M. S. 2013

    View details for PubMedID 23855951

  • Endocannabinoid Signaling and Long-Term Synaptic Plasticity ANNUAL REVIEW OF PHYSIOLOGY Heifets, B. D., Castillo, P. E. 2009; 71: 283-306

    Abstract

    Endocannabinoids (eCBs) are key activity-dependent signals regulating synaptic transmission throughout the central nervous system. Accordingly, eCBs are involved in neural functions ranging from feeding homeostasis to cognition. There is great interest in understanding how exogenous (e.g., cannabis) and endogenous cannabinoids affect behavior. Because behavioral adaptations are widely considered to rely on changes in synaptic strength, the prevalence of eCB-mediated long-term depression (eCB-LTD) at synapses throughout the brain merits close attention. The induction and expression of eCB-LTD, although remarkably similar at various synapses, are controlled by an array of regulatory influences that we are just beginning to uncover. This complexity endows eCB-LTD with important computational properties, such as coincidence detection and input specificity, critical for higher CNS functions like learning and memory. In this article, we review the major molecular and cellular mechanisms underlying eCB-LTD, as well as the potential physiological relevance of this widespread form of synaptic plasticity.

    View details for DOI 10.1146/annurev.physiol.010908.163149

    View details for Web of Science ID 000264489600014

    View details for PubMedID 19575681

  • Interneuron activity controls endocannabinoid-mediated presynaptic plasticity through calcineurin PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA Heifets, B. D., Chevaleyre, V., Castillo, P. E. 2008; 105 (29): 10250-10255

    Abstract

    Retrograde signaling by endocannabinoids (eCBs) mediates a widely expressed form of long-term depression at excitatory and inhibitory synapses (eCB-LTD), involving a reduction in neurotransmitter release. In the hippocampus, eCB-LTD occurs at interneuron (IN)-pyramidal cell (PC) synapses (I-LTD), and its induction requires a presynaptic reduction of cAMP/PKA signaling resulting from minutes of type 1 cannabinoid receptor (CB1R) activation. Although repetitive activity of glutamatergic synapses initiates the eCB mobilization required for I-LTD, it is unclear whether CB1R-containing GABAergic terminals are passive targets of eCBs or whether they actively contribute to induction. Here, we show that the minutes-long induction period for I-LTD may serve as a window to integrate associated spontaneous activity in the same IN receiving the retrograde eCB signal. Indeed, reducing spontaneous IN firing blocked I-LTD, which could be rescued with extra stimulation of inhibitory afferents. Moreover, cell pair recordings showed that a single IN expressed LTD onto a PC only if it was active during eCB signaling. Several methods of disrupting presynaptic Ca(2+) dynamics all blocked I-LTD, strongly suggesting that IN spikes regulate I-LTD by raising Ca(2+) at the nerve terminal. Finally, inhibiting the Ca(2+)-activated phosphatase, calcineurin, fully blocked I-LTD, but blocking another phosphatase did not. Our findings support a model where both CB1R signaling and IN activity shift the balance of kinase and phosphatase activity in the presynaptic terminal to induce I-LTD.

    View details for DOI 10.1073/pnas.0711880105

    View details for Web of Science ID 000257913200072

    View details for PubMedID 18632563

  • Endocannabinoid-mediated long-term plasticity requires cAMP/PKA signaling and RIM1 alpha NEURON Chevaleyre, V., Heifets, B. D., Kaeser, P. S., Sudhof, T. C., Purpura, D. P., Castillo, P. E. 2007; 54 (5): 801-812

    Abstract

    Endocannabinoids (eCBs) have emerged as key activity-dependent signals that, by activating presynaptic cannabinoid receptors (i.e., CB1) coupled to G(i/o) protein, can mediate short-term and long-term synaptic depression (LTD). While the presynaptic mechanisms underlying eCB-dependent short-term depression have been identified, the molecular events linking CB1 receptors to LTD are unknown. Here we show in the hippocampus that long-term, but not short-term, eCB-dependent depression of inhibitory transmission requires presynaptic cAMP/PKA signaling. We further identify the active zone protein RIM1alpha as a key mediator of both CB1 receptor effects on the release machinery and eCB-dependent LTD in the hippocampus. Moreover, we show that eCB-dependent LTD in the amygdala and hippocampus shares major mechanistic features. These findings reveal the signaling pathway by which CB1 receptors mediate long-term effects of eCBs in two crucial brain structures. Furthermore, our results highlight a conserved mechanism of presynaptic plasticity in the brain.

    View details for DOI 10.1016/j.neuron.2007.05.020

    View details for Web of Science ID 000247329900012

    View details for PubMedID 17553427

  • Chemical analysis of ecstasy pills JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION Baggott, M., Heifets, B., Jones, R. T., Mendelson, J., Sferios, E., Zehnder, J. 2000; 284 (17): 2190-2190

    View details for Web of Science ID 000090052600026

    View details for PubMedID 11056589