Enduring suppression of hippocampal long-term potentiation following traumatic brain injury in rat

S. Miyazaki, Y. Katayama, Bruce G Lyeth, L. W. Jenkins, D. S. DeWitt, S. J. Goldberg, P. G. Newlon, R. L. Hayes

Research output: Contribution to journalArticle

106 Scopus citations

Abstract

This study investigated changes in synaptic responses (population spike and population EPSP) of CA1 pyramidal cells of the rat hippocampus to stimulation of the Schaffer collateral/commissural pathways 2-3 h after traumatic brain injury (TBI). TBI was induced by a fluid percussion pulse delivered to the parietal epidural space resulting in loss of righting responses for 4.90-8.98 min. Prior to tetanic stimulation, changes observed after the injury included: (1) decreases in population spikes threshold but not EPSP thresholds; (2) deceases in maximal amplitude of population spikes as well as EPSPs. TBI also suppressed long-term potentiation (LTP), as evidenced by reductions in post-tetanic increases in population spikes as well as EPSPs. Since LTP may reflect processes involved in memory formation, the observed suppression of LTP may be an electrophysiological correlate of enduring memory deficits previously demonstrated in the same injury model.

Original languageEnglish (US)
Pages (from-to)335-339
Number of pages5
JournalBrain Research
Volume585
Issue number1-2
DOIs
StatePublished - Jul 10 1992
Externally publishedYes

    Fingerprint

Keywords

  • Brain injury
  • CA1
  • Hippocampus
  • Long-term potentiation
  • Rat
  • Traumatic brain injury

ASJC Scopus subject areas

  • Developmental Biology
  • Molecular Biology
  • Clinical Neurology
  • Neuroscience(all)

Cite this

Miyazaki, S., Katayama, Y., Lyeth, B. G., Jenkins, L. W., DeWitt, D. S., Goldberg, S. J., Newlon, P. G., & Hayes, R. L. (1992). Enduring suppression of hippocampal long-term potentiation following traumatic brain injury in rat. Brain Research, 585(1-2), 335-339. https://doi.org/10.1016/0006-8993(92)91232-4