Trent Anderson, PhD

Assistant Professor, Department of Basic Medical Sciences - The University of Arizona College of Medicine—Phoenix in partnership with Arizona State

UA Office Phone: (602) 827-2158
Office: Building ABC1, Room 428
Email: andersot@email.arizona.edu

Education:

Post-Doc: Neuroscience - Epilepsy, Parkinson's Disease; Stanford and Calgary University; 2002-2008

PhD; Queen's University; 2001

Background:

Dr. Anderson is a neuroscientist with an interest in the mechanisms that control cortical excitability in order to better understand how disruption of these processes influence disease states and provide avenues for therapeutic intervention. The pursuit of this research interest has provided the opportunity to study numerous neurological disorders. His PhD in Anatomy and Cell Biology from Queen’s University (Canada) focused on stroke and migraine research. While at the University of Calgary he was involved in translational studies in humans and animals to better understand the mechanisms of action and therapeutic potential of deep brain stimulation in the treatment of Parkinson’s disease and essential tremor. Most recently, Dr. Anderson studied at Stanford University examining how dysfunction of ionic and energy homeostasis may influence cortical hyperexcitability and the development of epilepsy. Currently Dr. Anderson can be found teaching Clinical Anatomy or within his lab investigating the role neurosteroids play in regulating cortical excitability.

Research Interests:

The brain is a fascinating lesson in duality – constantly balancing between the needs for diametrically opposed extremes. At its core it is an elegantly simplistic processing and computation center and yet its function results in the complicated behaviour, perception and reality we all experience. Built from simple single neurons the brain forms emergent networks that drive and govern our basic behaviour and how we perceive and interpret the world around us. Specifically, as a scientist I am intrigued by the duality of the balance the brain strikes between excitation and inhibition – tempering the need for excitatory activity to convey sensory and motor information with inhibitory activity that prevents run away excitation. Understanding the regulatory mechanisms that control this balance as well as the way disease states alter this balance has been the focus of my research career.

Did you know the brain consumes over 25% of the energy the body produces? This rate of consumption is 10 times greater than that of any other tissue. What is intriguing is given this extraordinary demand for energy the brain functions “inefficiently” – its excitatory activity is constantly being suppressed by an over-riding inhibitory activity. It is as if the brain is applying pressure to both the gas pedal and brake at the same time. The necessity for this inhibitory action is clearly evident as its loss or reduction has profound implication on the development and propagation of numerous disease states including epilepsy, Parkinson’s disease, stroke and migraine. In the cerebral cortex, the higher order processing center of the brain, inhibitory interneurons are responsible for this “brake”. These interneurons are a distinct and yet diverse group of specialized neurons with varying anatomical, pharmacologic and physiological properties that make them ideally situated to understand and manipulate this balance.

My research program combines aspects of cellular, synaptic and network neuroscience by using advanced tools in cellular physiology, neuropharmacology, imaging and molecular biology to elucidate mechanisms regulating excitability. Ongoing research points to neurosteroids as a prime candidate in regulating the balance between excitation and inhibition. Cortical neurons possess unique properties and sensitivities to neurosteroids that may be exploited to increase our understanding of the way the brain functions and as potential sources of therapeutic action. Steroids such as progesterone, pregnenonlone and dehydropiandrosterone are normally associated with their peripheral origin and action but have recently been shown to be de-novo synthesized in the brain itself. Specifically, several reports have indicated the ability of neurosteroids to alter both inhibitory (GABA) and excitatory (NMDA) function. Determining selective and novel pathways to up or down regulate the excitability of the brain may reveal significant sources of new therapeutic potential.

If you are interested in learning more or contributing to the research efforts in the lab please feel free to contact me by phone or email.

PubMed Link:

Search PubMed for a complete listing of Dr. Anderson's publications

Selected Publications:

  1. ANDERSON TR, Huguenard JR, Prince DA (in preparation). Site specific regulation of synaptic transmission in fast-spiking cortical interneurons by Na+/K+ ATPase
  2. ANDERSON TR, Huguenard JR, Prince DA (in preparation). The differential effect of Na+/K+ ATPase blockade on cortical layer V neurons
  3. Kiss ZHT, ANDERSON TR. (2007) Cellular mechanisms of action of therapeutic brain stimulation, in Bronzino J and DiLorenzo DJ (Eds): Neuroenginerring, CRC Press/Taylor and Francis
  4. Iremonger KJ, ANERSON TR, Hu B, Kiss ZH. (2006) Cellular mechanisms preventing sustained activation of cortex during subcortical high-frequency stimulation. J Neurophysiol. 96(2): 613-621
  5. 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. 26(3):841-850.
  6. ANDERSON TR, Jarvis CR, Biedermann AJ, Molnar C, Andrew RD. (2005) Blocking the anoxic depolarization protects without functional compromise following simulated stroke in cortical brain slices. J Neurophysiol. 93(2):963-79
  7. ANDERSON TR, Hu B, Pittman Q, Kiss ZHT. (2004) Mechanisms of deep brain stimulation: an intracellular study in rat thalamus. J Physiol. 559(1):301-13
  8. Kiss ZH, ANDERSON TR, Hansen T, Kirstein D, Suchowersky O, Hu B. (2003) Neural substrates of microstimulation-evoked tingling: a chronaxie study in human somatosensory thalamus. Eur J Neurosci. 18(3):728-32
  9. Andrew, R.D., Biedermann, A.J., ANDERSON, T.R., Jarvis, C.R. (2002) Imaging and preventing spreading depression independent of cerebral blood flow. In: Brain Activation and CBF Control. Eds M. Tomita, I. Kanno and E. Hamel. Elsevier Sciences.
  10. ANDERSON TR, Andrew RD. (2002) Spreading depression: imaging and blockade in the rat neocortical brain slice. J Neurophysiol. 88(5):2713-25