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Author Notes:

*Correspondence: James W. Grau, Cellular and Behavioral Neuroscience, Department of Psychology, Texas A&M University, College Station, TX 77843-4235, USA e-mail: j-grau@tamu.edu

The Guest Associate Editor Shawn Hochman declares that, despite being affiliated to the same institution as author Sandra M. Garraway, the review process was handled objectively and no conflict of interest exists.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Subjects:

Research Funding:

Preparation of this paper was supported by grants from Mission Connect to James W. Grau, Michelle A. Hook, and Sandra M. Garraway, NS081606 to Sandra M. Garraway, Michelle A. Hook, and James W. Grau, DA031197 to Michelle A. Hook, James W. Grau, and Sandra M. Garraway, and NS069537 to Adam R. Ferguson and James W. Grau.

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Neurosciences
  • Neurosciences & Neurology
  • plasticity
  • learning
  • inflammation
  • spinal cord injury
  • nociception
  • BDNF
  • TNF
  • opioid
  • LONG-TERM POTENTIATION
  • METABOTROPIC GLUTAMATE RECEPTORS
  • LAMINA-II NEURONS
  • PROTEIN-KINASE-C
  • BDNF-INDUCED FACILITATION
  • CHRONIC NEUROPATHIC PAIN
  • GLIAL TNF-ALPHA
  • NEUROTROPHIC FACTOR
  • NMDA RECEPTOR
  • SYNAPTIC PLASTICITY

Metaplasticity and behavior: how training and inflammation affect plastic potential within the spinal cord and recovery after injury

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Journal Title:

Frontiers in Neural Circuits

Volume:

Volume 8, Number SEP

Publisher:

, Pages 100-100

Type of Work:

Article | Final Publisher PDF

Abstract:

Research has shown that spinal circuits have the capacity to adapt in response to training, nociceptive stimulation and peripheral inflammation. These changes in neural function are mediated by physiological and neurochemical systems analogous to those that support plasticity within the hippocampus (e.g., long-term potentiation and the NMDA receptor). As observed in the hippocampus, engaging spinal circuits can have a lasting impact on plastic potential, enabling or inhibiting the capacity to learn. These effects are related to the concept of metaplasticity. Behavioral paradigms are described that induce metaplastic effects within the spinal cord. Uncontrollable/unpredictable stimulation, and peripheral inflammation, induce a form of maladaptive plasticity that inhibits spinal learning. Conversely, exposure to controllable or predictable stimulation engages a form of adaptive plasticity that counters these maladaptive effects and enables learning. Adaptive plasticity is tied to an up-regulation of brain derived neurotrophic factor (BDNF). Maladaptive plasticity is linked to processes that involve kappa opioids, the metabotropic glutamate (mGlu) receptor, glia, and the cytokine tumor necrosis factor (TNF). Uncontrollable nociceptive stimulation also impairs recovery after a spinal contusion injury and fosters the development of pain (allodynia). These adverse effects are related to an up-regulation of TNF and a down-regulation of BDNF and its receptor (TrkB). In the absence of injury, brain systems quell the sensitization of spinal circuits through descending serotonergic fibers and the serotonin 1A (5HT 1A) receptor. This protective effect is blocked by surgical anesthesia. Disconnected from the brain, intracellular Cl- concentrations increase (due to a down-regulation of the cotransporter KCC2), which causes GABA to have an excitatory effect. It is suggested that BDNF has a restorative effect because it up-regulates KCC2 and re-establishes GABA-mediated inhibition.

Copyright information:

© 2014 Grau, Huie, Lee, Hoy, Huang, Turtle, Strain, Baumbauer, Miranda, Hook, Ferguson and Garraway.

This is an Open Access work distributed under the terms of the Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/).
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