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This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: 102/4/2396    most recent 00095.2009v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Tan, A. M. Articles by Hains, B. C. PubMed PubMed Citation Articles by Tan, A. M. Articles by Hains, B. C.

RESEARCH-ARTICLE

Dendritic Spine Remodeling After Spinal Cord Injury Alters Neuronal Signal Processing

Departments of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, and Rehabilitation Research Center, Veterans Affairs Connecticut Healthcare System, West Haven, Connecticut

Submitted 2 February 2009; accepted in final form 12 August 2009

ABSTRACT

Central sensitization, a prolonged hyperexcitability of dorsal horn nociceptive neurons, is a major contributor to abnormal pain processing after spinal cord injury (SCI). Dendritic spines are micron-sized dendrite protrusions that can regulate the efficacy of synaptic transmission. Here we used a computational approach to study whether changes in dendritic spine shape, density, and distribution can individually, or in combination, adversely modify the input–output function of a postsynaptic neuron to create a hyperexcitable neuronal state. The results demonstrate that a conversion from thin-shaped to more mature, mushroom-shaped spine structures results in enhanced synaptic transmission and fidelity, improved frequency-following ability, and reduced inhibitory gating effectiveness. Increasing the density and redistributing spines toward the soma results in a greater probability of action potential activation. Our results demonstrate that changes in dendritic spine morphology, documented in previous studies on spinal cord injury, contribute to the generation of pain following SCI.