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About Sickkids
About SickKids

Steve Prescott, MD, PhD

Research Institute
Neurosciences & Mental Health

University of Toronto
Assistant Professor
Department of Physiology

Phone: 416-813-7654 ext. 329877
Fax: 416-813-7921
Email: steve.prescott@sickkids.ca

For more information, visit:

The Prescott Lab

Brief Biography

I obtained my MD and PhD from McGill University in 2005. My doctoral research focused on the investigation of pain processing using electrophysiology, pharmacology, and cellular imaging. I then did post-doctoral training in computational neuroscience at the Salk Institute with Terry Sejnowski. In 2008, I set up my own lab at the University of Pittsburgh with the intent of combining a range of experimental and computational tools to investigate pain processing. In 2012, my lab moved to SickKids.

Research Interests

Our ultimate goal is to uncover how the nervous system processes pain-related sensory information and how chronic pain arises from aberrations in that processing. To that end, we investigate the biophysical basis for neural information processing at the cellular and network levels. Those findings have broad applications but we also consider the specific consequences of neural information processing for pain. Thus, through a two-step process —linking biophysics with information processing, and information processing with pain— we hope to gain a detailed, robust understanding of the biophysical (molecular) basis of chronic pain.

Our approach is a multidisciplinary one involving electrophysiology, calcium imaging, and optogenetics together with computational simulations and rigorous mathematical analysis.

External Funding

  • CIHR New Investigator Salary Award - Computational deconstruction of pain processing 
  • NSERC Discovery Grant - Neural dynamics: their nonlinear basis and computational consequences 
  • Mallinckrodt Scholar Program - Using optogenetics to probe how disruption of neural coding causes neuropathic pain 
  • NIH R21 NS074146 - Computational investigation of neuropathic changes in primary afferent excitability 
  • NIH R01 NS076706 - Biophysical mechanisms regulating synchrony transfer in somatosensory cortex


  • 53rd Mallinckrodt Scholar
  • Rita Allen Foundation Scholar in Pain


Ratté S, Hong SH, De Schutter E, Prescott SA. Impact of neuronal properties on network coding: roles of spike initiation dynamics and robust synchrony transfer. Neuron 2013; 78: 758-772.

Prescott SA, Ratté S. Pain processing by spinal microcircuits: afferent combinatorics. Curr. Opin. Neurobiol. 2012; 22: 631-639.

Rho Y-A, Prescott SA. Identifying molecular pathologies sufficient to cause neuropathic change in primary somatosensory afferent excitability using dynamical systems theory. PLoS Comput. Biol. 2012; 8; e1002524.

Hong S, Ratté S, Prescott SA, De Schutter E. Single neuron firing properties impact correlation-based population coding. J. Neurosci 2012; 32: 1413-1428.

Ratté S, Prescott SA. ClC-2 channels regulate neuronal excitability, not intracellular chloride levels. J. Neurosci. 2011; 31: 15838-15843.

Coggan JS, Ocker GK, Sejnowski TJ, Prescott SA. Explaining pathological changes in axonal excitability through dynamical analysis of conductance-based models. J. Neural Eng. 2011; 8: 065002.

Doyon N, Prescott SA, Castonguay A, Godin AG, Kröger A, De Koninck Y. Efficacy of synaptic inhibition depends on multiple, dynamically interacting mechanisms implicated in chloride homeostasis.  PLoS Comput. Biol. 2011; 7; e1002149.

Coggan JS, Prescott SA, Bartol TM, Sejnowski TJ. Imbalance of ionic conductances contributes to diverse symptoms of demyelination. Proc. Natl. Acad. Sci. USA 2010; 107: 20602-20609.