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Timothy Angelotti MD, PhD

Academic Appointments

  • Associate Professor of Anesthesiology, Perioperative and Pain Medicine at the Stanford University Medical Center

Contact Information

  • Clinical Offices
    Department of Anesthesia 300 Pasteur Dr H3580 MC 5640 Stanford, CA 94305
    Tel Work (650) 498-7525 Fax (650) 725-8544
  • Academic Offices
    Personal Information
    Email Tel (650) 498-7525 Tel (650) 736-2030
    Alternate Contact
    Erin Reiland Administrative Assistant Tel Work 723-7442
    Not for medical emergencies or patient use

Professional Overview

Clinical Focus

  • Anesthesia
  • Critical Care

Academic Appointments

Administrative Appointments

  • Medical Director - Critical Care Transport, Stanford Life Flight (2000 - present)
  • Associate Medical Director, MICU, Stanford University Medical Center (2005 - present)

Honors and Awards

  • Best of Meeting Award (82nd Annual IARS Congress), IARS (2008)
  • Alexander von Humboldt Foundation Post-Doctoral Fellowship, Alexander von Humboldt Foundation (1995-1996)
  • Dean's Award for Research Excellence, University of Michigan (1994)

Professional Education

Internship: St Joseph's Mercy Hospital MI (1995)
Residency: Duke University Medical Center NC (1999)
Fellowship: Stanford University School of Medicine CA (2000)
Board Certification: Anesthesia, American Board of Anesthesiology (2000)
Board Certification: Critical Care Medicine, American Board of Anesthesiology (2001)
Medical Education: University of Michigan School of Medicine MI (1994)
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Graduate and Fellowship Program Affiliations

Scientific Focus

Current Research and Scholarly Interests

The sympathetic nervous system (SNS) functions as an integrative peripheral nervous system to regulate vital organ function, in part by release of norepinephrine (NE). Disease states as varied as Parkinson’s disease, spinal cord injury, diabetes, heart failure, and sepsis can all lead to dysfunction of the SNS and patient morbidity. Feedback modulation of NE release occurs by activation of alpha2A and alpha2C adrenergic receptors (ARs) on sympathetic neurons. Neuropharmacological differences between these two autoreceptors are not completely known, thus limiting development of specific drugs for disease treatment.

Modulation of sympathetic neuron signaling occurs by feedback inhibition of neurotransmitter release (autoreceptors), mediated in part via alpha2A and/or alpha2C adrenergic receptors. Previous research suggests that these two AR subtypes may have overlapping but unique physiological roles in neuronal signaling; however the basis for these differences is not completely known. Cellular localization is an important determinant of specialized function between homologous receptors. Preliminary data in cultured sympathetic ganglion neurons (SGN) and other cell types have found different temporal and spatial components to alpha2A&C AR localization and trafficking. These differences may relate to characteristics of SGN in culture (e.g. neurotransmitter phenotype) and thus may be important determinants of differential alpha2A&C AR modulation of neurotransmitter release. Using an array of molecular and cellular approaches and single cell amperometric analysis of neurotransmitter release, it should be possible to further delineate the interplay between protein structure, cellular localization, and physiological function of each receptor subtype. Resultant discoveries will be relevant to other similar neuromodulatory systems involved in pain and neural processing, including cannabinoid, opiate, and metabotropic glutamate receptors.


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Publication Topics

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