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Genom Data. 2015 Oct 23;6:249-52. doi: 10.1016/j.gdata.2015.10.005. eCollection 2015 Dec.

Transcriptional changes in sensory ganglia associated with primary afferent axon collateral sprouting in spared dermatome model.

Author information

1
Department of Anatomical Sciences and Neurobiology, University of Louisville, Louisville, KY 40202, United States ; Kentucky Spinal Cord Injury Research Center (KSCIRC), University of Louisville, Louisville, KY 40202, United States ; Kentucky Biomedical Research Infrastructure Network Bioinformatics Core, University of Louisville, Louisville, KY 40292, United States.
2
Department of Anatomical Sciences and Neurobiology, University of Louisville, Louisville, KY 40202, United States ; Kentucky Spinal Cord Injury Research Center (KSCIRC), University of Louisville, Louisville, KY 40202, United States.
3
Wolfson Centre for Age Related Diseases, King's College, London, UK.
4
Department of Anatomical Sciences and Neurobiology, University of Louisville, Louisville, KY 40202, United States ; Kentucky Spinal Cord Injury Research Center (KSCIRC), University of Louisville, Louisville, KY 40202, United States ; Department of Anesthesiology and Perioperative Medicine, University of Louisville, Louisville, KY 40202, United States.
5
Miami Project to Cure Paralysis, Department of Neurological Surgery and Neurology, University of Miami Miller School of Medicine, Miami, FL, 33136, United States ; Christopher and Dana Reeve Foundation International Consortium on Spinal Cord Injury Research.
6
Christopher and Dana Reeve Foundation International Consortium on Spinal Cord Injury Research ; Department of Neurobiology and Behavior, State University of New York at Stony Brook, Stony Brook, NY 11794, United States.
7
Christopher and Dana Reeve Foundation International Consortium on Spinal Cord Injury Research ; Laboratory of Genetics, The Salk Institute, La Jolla, CA 92037, United States.
8
Department of Physiological Sciences, University of Florida, Gainesville, FL 32210, United States ; McKnight Brain Institute at the University of Florida, Gainesville, FL 32611, United States.
9
Weill Medical College of Cornell University, Brain and Mind Research Institute, New York, NY, United States ; Burke Medical Research Institute, White Plains, NY 10605, United States.
10
Kentucky Biomedical Research Infrastructure Network Bioinformatics Core, University of Louisville, Louisville, KY 40292, United States ; Department of Computer Engineering and Computer Science, University of Louisville, Louisville, KY 40292, United States.
11
Department of Anatomical Sciences and Neurobiology, University of Louisville, Louisville, KY 40202, United States ; Kentucky Spinal Cord Injury Research Center (KSCIRC), University of Louisville, Louisville, KY 40202, United States ; Department of Neurosurgery, University of Louisville, Louisville, KY 40202, United States.

Abstract

Primary afferent collateral sprouting is a process whereby non-injured primary afferent neurons respond to some stimulus and extend new branches from existing axons. Neurons of both the central and peripheral nervous systems undergo this process, which contributes to both adaptive and maladaptive plasticity (e.g., [1], [2], [3], [4], [5], [6], [7], [8], [9]). In the model used here (the "spared dermatome" model), the intact sensory neurons respond to the denervation of adjacent areas of skin by sprouting new axon branches into that adjacent denervated territory. Investigations of gene expression changes associated with collateral sprouting can provide a better understanding of the molecular mechanisms controlling this process. Consequently, it can be used to develop treatments to promote functional recovery for spinal cord injury and other similar conditions. This report includes raw gene expression data files from microarray experiments in order to study the gene regulation in spared sensory ganglia in the initiation (7 days) and maintenance (14 days) phases of the spared dermatome model relative to intact ("naïve") sensory ganglia. Data has been deposited into GEO (GSE72551).

KEYWORDS:

Axon growth; Axonal plasticity; Nerve injury; Pain; Transcriptomics

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