Trent R. Anderson

Contact:

University of Arizona College of Medicine - Phoenix ABC-1 Building 425 North 5th Street, Phoenix, AZ 85004
Building
ABC 1
Associate Professor
Associate Professor - Basic Medical Sciences
Faculty
Basic Medical Sciences

Education

  • Postdoctoral Fellowship: Neuroscience, Stanford University, 2008
  • Postdoctoral Fellowship: Neuroscience, University of Calgary, 2005
  • PhD: Anatomy and Cell Biology, Queen's University, 2001

Representative Recent Publications

  • Bharadwaj VN, Copeland C, Mathew E, Newbern J, Anderson TR, Lifshitz J, Kodibagkar VD & Stabenfeldt SE (2020). Sex-Dependent Macromolecule and Nanoparticle Delivery in Experimental Brain Injury. Tissue Eng Part A. Vol. 26(13-14), 688-701.
  • Kiss ZHT & Anderson TR (2007). Cellular mechanisms of action of therapeutic brain stimulation, in Bronzino J and DiLorenzo DJ (Eds). CRC Press/Taylor and Francis.
  • Iremonger KJ, Anderson TR, Hu B & Kiss ZH (2006). Cellular mechanisms preventing sustained activation of cortex during subcortical high-frequency stimulation. J Neurophysiol. Vol. 96(2), 613-621.
  • Anderson TR, Hu B, Iremonger K & Kiss ZH (2006). Selective attenuation of afferent synaptic transmission as a mechanism of thalamic deep brain stimulation-induced tremor arrest. J Neurosci. Vol. 26(3), 841-850.
  • Nichols J, Perez R, Wu C, Adelson PD & Anderson T (2015). Traumatic brain injury induces rapid enhancement of cortical excitability in juvenile rats. Verson 2. CNS Neurosci Ther. Vol. 21(2), 193-203.
Research Interests
Traumatic Brain Injury, Psychiatric Disease, Neuroscience, Neurophysiology, Neurodegenerative Diseases, Neuroanatomy, Migraine, Electrophysiology, Diagnostic Imaging, Developmental, cell and molecular biology, Developmental Disabilities, Cancer, Anatomy
Research Summary

Dr. Anderson’s laboratory is focused on understanding how mechanisms that regulate cortical excitability influence the development of neurological disease. Specifically, my laboratory utilizes electrophysiological, neuroimaging, optogenetic and behavioral approaches to examine the interface between traumatic brain injury (TBI), migraine and epilepsy. While with more severe TBI the network is predisposed to the development of epilepsy, many patients that experience more mild TBI develop long-term persistent headaches, especially migraine. The underlying mechanisms of post-traumatic epilepsy (PTE) and post-traumatic headache (PTH) are poorly understood and difficult to treat. My laboratory aims to improve understanding of these disease and identify and develop new efficacious therapies.