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Investigations on Alterations of Hippocampal Circuit Function Following Mild Traumatic Brain Injury
10:59

Investigations on Alterations of Hippocampal Circuit Function Following Mild Traumatic Brain Injury

Published on: November 19, 2012

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Repeated mild traumatic brain injury causes chronic neuroinflammation, changes in hippocampal synaptic plasticity,

Stephanie L Aungst1, Shruti V Kabadi1, Scott M Thompson2

  • 1Department of Anesthesiology, Shock, Trauma, and Anesthesiology Research (STAR) Center, University of Maryland School of Medicine, Heath Sciences Facility 2 (HSF2), Baltimore, Maryland, USA.

Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism
|April 24, 2014
PubMed

Insights

Repeated mild traumatic brain injury (mTBI) causes significant neuroinflammation and neuronal loss in rat hippocampus. This leads to impaired synaptic plasticity and cognitive deficits, highlighting long-term consequences of head trauma.

Area of Science:

  • Neuroscience
  • Traumatic Brain Injury Research
  • Neuroinflammation

Background:

  • Repeated mild traumatic brain injury (mTBI) is linked to persistent cognitive and psychiatric issues, alongside neurodegeneration.
  • The precise biological mechanisms underlying these chronic effects remain incompletely understood.

Purpose of the Study:

  • To investigate the histologic, neurophysiological, and cognitive consequences of single versus repeated mTBI.
  • To elucidate the impact of mTBI on hippocampal function and synaptic transmission.

Main Methods:

  • Utilized the rat lateral fluid percussion (LFP) model to induce single or repeated (three) mTBIs.
  • Assessed neuronal cell loss, microglial activation, long-term potentiation (LTP), and receptor-mediated responses (NMDA, AMPA) in hippocampal slices.
  • Evaluated cognitive function using the Morris water maze (MWM) and novel object recognition (NOR) tests.

Main Results:

  • Repeated mTBI resulted in significant neuronal loss and increased microglial activation in the hippocampus by post-injury day 28.
  • Long-term potentiation (LTP) was impaired, and N-Methyl-D-aspartate (NMDA) receptor responses were attenuated following repeated mTBI.
  • Single mTBI elicited LTP, with greater potentiation in the ipsilateral hippocampus, while repeated mTBI induced cognitive deficits in MWM and NOR tests.

Conclusions:

  • Repeated mTBI induces chronic neuroinflammation and neurodegeneration in the hippocampus.
  • These pathological changes correlate with impaired hippocampal synaptic function and long-lasting cognitive deficits.

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