NIH Biosketch available OnlineTimothy Angelotti MD, PhD
- Associate Professor - Med Center Line, Anesthesia
Contact Information
- Clinical Offices
Department of Anesthesia 300 Pasteur Dr H3580 MC 5640 Stanford, CA 94305 Telephone Work (650) 498-7525 Fax (650) 725-8544
- Academic Offices
Personal Information Email timangel@stanford.edu Tel (650) 498-7525, (650) 736-2030Administrative Contact Erin Reiland Administrative Assistant Email ereiland@stanford.edu Tel Work 723-7442Not for medical emergencies or patient use
Clinical Focus
- Anesthesia
- Critical Care
Administrative Appointments
- Associate Medical Director, MICU, Stanford University Medical Center , (2005– present )
- Associate Medical Director, Stanford Life Flight , (2000– present )
Honors and Awards
- 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
- Board Certification: Anesthesia, American Board of Anesthesiology (2000)
- Board Certification: Critical Care Medicine, American Board of Anesthesiology (2001)
- SUMC - Graduate Medical Education (2000) CA
- Duke University Medical Center (1999) NC
- St. Joseph's Mercy Hospital (1995) MI
- University of Michigan School of Medicine (1994) MI
- MD, University of Michigan (1994)
- PhD, University of Michigan Pharmacology (1994)
Postdoctoral Advisees
Graduate & Fellowship Program Affiliations
Web Site Links
Research 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.
Publications
- J Biol Chem. 2009; (19): 13233-43
- Neuroscience. 2008; (4): 1268-77
- Anesth Analg. 2007; (1): 229-30
- Anesth Analg. 2007; (4): 1168; author reply 1169
- Seminars in Anesthesia, Perioperative Medicine and Pain. 2007; (1): 28-34
- Epilepsy Res. 2007; (2): 137-50
- Air Med J. 2006 Mar-Apr; (2): 74-8; discussion 78-80
- Neuropharmacology. 2006; (3): 397-413
- J Clin Anesth. 2005; (6): 478-81
- Mol Pharm (in preparation).. 2004;
- J Clin Anesth. 2004; (6): 465-8
- Anesth Analg. 2003; (4): 1237
- Lupus. 2002; (5): 325-8
- Cell Growth Differ. 1998; (3): 247-56
- Mol Cells. 1998; (1): 2-11
- Epilepsy Res Suppl. 1996; 177-85
- Mol Pharmacol. 1996; (1): 185-95
- FEBS Lett. 1996; (2-3): 331-7
- J Biol Chem. 1995; (45): 27380-8
- AxoBits. 1994; (15): 6-8
- J Neurosci. 1993; (4): 1418-28
- J Neurosci. 1993; (4): 1429-40
- Mol Pharmacol. 1993; (6): 1202-10
- Epilepsy Res Suppl. 1992; 265-77
- Brain Res Mol Brain Res. 1992; (1-2): 173-8
- Mol Pharmacol. 1992; (5): 872-81
- Bioconjug Chem. 1991 Nov-Dec; (6): 466-74