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Turtle JD, Strain MM, Reynolds JA, et al. Pain Input After Spinal Cord Injury (SCI) Undermines Long-Term Recovery and Engages Signal Pathways That Promote Cell Death. Front Syst Neurosci. 2018;12:27doi: 10.3389/fnsys.2018.00027.
Turtle, J. D., Strain, M. M., Reynolds, J. A., Huang, Y. J., Lee, K. H., Henwood, M. K., Garraway, S. M., & Grau, J. W. (2018). Pain Input After Spinal Cord Injury (SCI) Undermines Long-Term Recovery and Engages Signal Pathways That Promote Cell Death. Frontiers in systems neuroscience, 1227. https://doi.org/10.3389/fnsys.2018.00027
Turtle, Joel D, et al. "Pain Input After Spinal Cord Injury (SCI) Undermines Long-Term Recovery and Engages Signal Pathways That Promote Cell Death." Frontiers in systems neuroscience vol. 12 (2018): 27. doi: https://doi.org/10.3389/fnsys.2018.00027
Turtle JD, Strain MM, Reynolds JA, Huang YJ, Lee KH, Henwood MK, Garraway SM, Grau JW. Pain Input After Spinal Cord Injury (SCI) Undermines Long-Term Recovery and Engages Signal Pathways That Promote Cell Death. Front Syst Neurosci. 2018 Jun 21;12:27. doi: 10.3389/fnsys.2018.00027. eCollection 2018. PMID: 29977195; PMCID: PMC6021528.
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Front Syst Neurosci. 2018 Jun 21;12:27. doi: 10.3389/fnsys.2018.00027. eCollection 2018.

Pain Input After Spinal Cord Injury (SCI) Undermines Long-Term Recovery and Engages Signal Pathways That Promote Cell Death.

Frontiers in systems neuroscience

Joel D Turtle, Misty M Strain, Joshua A Reynolds, Yung-Jen Huang, Kuan H Lee, Melissa K Henwood, Sandra M Garraway, James W Grau

Affiliations

  1. Lab of Dr. James Grau, Department of Psychology, Cellular and Behavioral Neuroscience, Texas A&M University, College Station, TX, United States.
  2. United States Army Institute of Surgical Research, JBSA-Fort Sam Houston, San Antonio, TX, United States.
  3. Department of Physiology, Emory University School of Medicine, Atlanta, GA, United States.

PMID: 29977195 PMCID: PMC6021528 DOI: 10.3389/fnsys.2018.00027

Abstract

Pain (nociceptive) input caudal to a spinal contusion injury increases tissue loss and impairs long-term recovery. It was hypothesized that noxious stimulation has this effect because it engages unmyelinated pain (C) fibers that produce a state of over-excitation in central pathways. The present article explored this issue by assessing the effect of capsaicin, which activates C-fibers that express the transient receptor potential vanilloid receptor-1 (TRPV1). Rats received a lower thoracic (T11) contusion injury and capsaicin was applied to one hind paw the next day. For comparison, other animals received noxious electrical stimulation at an intensity that engages C fibers. Both forms of stimulation elicited similar levels of

Keywords: apoptosis; capsaicin; cell death; pain; pyroptosis; recovery; spinal cord injury

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