Computational Basis of Pain Processing

Our research focuses on how neurons process information and how that processing impacts pain perception under normal and pathological conditions. This research is motivated by the view that deciphering how the processing of sensory information becomes deranged following neuropathy will help us understand and treat the perceptual abnormalities (e.g. allodynia and hyperalgesia) associated with neuropathic pain.

One specific goal is to unravel the neural circuitry in the superficial dorsal horn of the spinal cord using a combination of electrophysiology, retrograde labeling, and calcium imaging. Given the intrinsic cellular properties and synaptic connectivity, the next goal is to characterize the flow of information through the circuit. Computer simulations will help determine precisely how changes in cellular and synaptic properties impact circuit function, leading to specific predictions that will be tested experimentally. Reversible inactivation of circuit components and pharmacological modulation will be tested in vivo in order to help translate physiological knowledge into behaviorally relevant understanding that may have clinical implications.

Sample Publications:

Pain processing by spinal microcircuits: afferent combinatorics.
Prescott SA, Ratté S.
Curr Opin Neurobiol. 2012 Mar 10.

Single neuron firing properties impact correlation-based population coding.
Hong S, Ratté S, Prescott SA, De Schutter E.
J Neurosci. 2012 Jan 25;32(4):1413-28.

Explaining pathological changes in axonal excitability through dynamical analysis of conductance-based models.
Coggan JS, Ocker GK, Sejnowski TJ, Prescott SA.
J Neural Eng. 2011 Dec;8(6):065002.

ClC-2 channels regulate neuronal excitability, not intracellular chloride levels.
Ratté S, Prescott SA.
J Neurosci. 2011 Nov 2;31(44):15838-43.

Efficacy of synaptic inhibition depends on multiple, dynamically interacting mechanisms implicated in chloride homeostasis.
Doyon N, Prescott SA, Castonguay A, Godin AG, Kröger H, De Koninck Y.
PLoS Comput Biol. 2011 Sep;7(9):e1002149.

Imbalance of ionic conductances contributes to diverse symptoms of demyelination.
Coggan JS, Prescott SA, Bartol TM, Sejnowski TJ.
Proc Natl Acad Sci U S A. 2010 Nov 30;107(48):20602-9.

Chloride regulation in the pain pathway.
Price TJ, Cervero F, Gold MS, Hammond DL, Prescott SA.
Brain Res Rev. 2009 Apr;60(1):149-70.

Spike-rate coding and spike-time coding are affected oppositely by different adaptation mechanisms.
Prescott SA, Sejnowski TJ.
J Neurosci. 2008 Dec 10;28(50):13649-61.

Biophysical basis for three distinct dynamical mechanisms of action potential initiation.
Prescott SA, De Koninck Y, Sejnowski TJ.
PLoS Comput Biol. 2008 Oct;4(10):e1000198.

Nonlinear interaction between shunting and adaptation controls a switch between integration and coincidence detection in pyramidal neurons.
Prescott SA, Ratté S, De Koninck Y, Sejnowski TJ.
J Neurosci. 2006 Sep 6;26(36):9084-97.

Trans-synaptic shift in anion gradient in spinal lamina I neurons as a mechanism of neuropathic pain.
Coull JA, Boudreau D, Bachand K, Prescott SA, Nault F, Sík A, De Koninck P, De Koninck Y.
Nature. 2003 Aug 21;424(6951):938-42.

Gain control of firing rate by shunting inhibition: roles of synaptic noise and dendritic saturation.
Prescott SA, De Koninck Y.
Proc Natl Acad Sci U S A. 2003 Feb 18;100(4):2076-81.

PubMed Search for "Prescott SA"

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