Prescott, Steven A.|
Assistant Professor, Neurobiology
M.D. Ph.D., McGill University (2005)
Address: W1455 BSTWR
200 Lothrop Street
Pittsburgh, PA 15213-2536
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.
Pain processing by spinal microcircuits: afferent combinatorics.
Single neuron firing properties impact correlation-based population coding.
Explaining pathological changes in axonal excitability through dynamical analysis of conductance-based models.
ClC-2 channels regulate neuronal excitability, not intracellular chloride levels.
Efficacy of synaptic inhibition depends on multiple, dynamically interacting mechanisms implicated in chloride homeostasis.
Imbalance of ionic conductances contributes to diverse symptoms of demyelination.
Chloride regulation in the pain pathway.
Spike-rate coding and spike-time coding are affected oppositely by different adaptation mechanisms.
Biophysical basis for three distinct dynamical mechanisms of action potential initiation.
Nonlinear interaction between shunting and adaptation controls a switch between integration and coincidence detection in pyramidal neurons.
Trans-synaptic shift in anion gradient in spinal lamina I neurons as a mechanism of neuropathic pain.
Gain control of firing rate by shunting inhibition: roles of synaptic noise and dendritic saturation.
© Copyright 2001 - University
of Pittsburgh Department of Neurobiology