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Author Notes:

Correspondence should be addressed to: Professor Garrett B. Stanley, Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, 313 Ferst Drive, Atlanta, GA 30332. E-mail: garrett.stanley@bme.gatech.edu.

Author contributions: M.-C.D., E.H.L., and G.B.S. designed research; M.-C.D. and Q.W. performed research; M.-C.D. and Q.W. analyzed data; M.-C.D., E.H.L., and G.B.S. wrote the paper.

Subjects:

Research Funding:

This work was supported by NINDS Grant R01 NS48285.

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Neurosciences
  • Neurosciences & Neurology
  • RECEPTIVE-FIELD PROPERTIES
  • MOUSE BARREL CORTEX
  • SPREADING DEPRESSION
  • SOMATOSENSORY CORTEX
  • FUNCTIONAL RECOVERY
  • CEREBRAL-ISCHEMIA
  • IN-VIVO
  • MOLECULAR-MECHANISMS
  • SENSORY RESPONSES
  • NEURONAL-ACTIVITY

Cortical Excitation and Inhibition following Focal Traumatic Brain Injury

Tools:

Journal Title:

Journal of Neuroscience Nursing

Volume:

Volume 31, Number 40

Publisher:

, Pages 14085-14094

Type of Work:

Article | Final Publisher PDF

Abstract:

Cortical compression can be a significant problem in many types of brain injuries, such as brain trauma, localized brain edema, hematoma, focal cerebral ischemia, or brain tumors. Mechanical and cellular alterations can result in global changes in excitation and inhibition on the neuronal network level even in the absence of histologically significant cell injury, often manifesting clinically as seizures. Despite the importance and prevalence of this problem, however, the preciseelectro physiological effects of brain injury have not been well characterized. In this study, the changes in electrophysiology were characterized following sustained cortical compression usinglarge-scale, multi electrode measurement of multiun it activity in primary somatosensory cortexinasensory-evoked, in vivoanimal model. Immediately following the initiation of injury at a distal site, there was a period of suppression of the evoked response in the rat somatosensory cortex, followed by hyper-excitability that was accompanied by an increase in the spatial extent of cortical activation. Paired-pulse tactile stimulation revealed a dramatic shift in the excitatory/inhibitory dynamics, suggesting a longer term hyperexcitability of the cortical circuit following the initial suppression that could be linked to the disruption of one or more inhibitory mechanisms of the thalamocortical circuit. Together, our results showed that the use of a sensory-evoked response provided a robust and repeatable functional marker of the evolution of the consequences of mild injury, serving as an important step toward in vivo quantification of alterations in excitation and inhibition in the cortex in the setting of traumatic brain injury.

Copyright information:

© 2011 the authors.

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