Presynaptic excitability changes following traumatic brain injury in the rat

Thomas M. Reeves, Chang Q. Kao, Linda L. Phillips, Ross Bullock, John T. Povlishock

Research output: Contribution to journalArticle

42 Citations (Scopus)

Abstract

Pathological processes affecting presynaptic terminals may contribute to morbidity following traumatic brain injury (TBI). Posttraumatic widespread neuronal depolarization and elevated extracellular potassium and glutamate are predicted to alter the transduction of action potentials in terminals into reliable synaptic transmission and postsynaptic excitation. Evoked responses to orthodromic single- and paired-pulse stimulation were examined in the CA1 dendritic region of hippocampal slices removed from adult rats following fluid percussion TBI. The mean duration of the extracellularly recorded presynaptic volley (PV) increased from 1.08 msec in controls to 1.54 msec in slices prepared at 1 hr postinjury. There was a time-dependent recovery of this injury effect, and PV durations at 2 and 7 days postinjury were not different from controls. In slices removed at 1 hr postinjury, the initial slopes of field excitatory postsynaptic potentials (fEPSPs) were reduced to 36% of control values, and input/output plots revealed posttraumatic deficits in the transfer of excitation from pre- to postsynaptic elements. Manipulating potassium currents with 1.0 mM tetraethylammonium or elevating potassium ion concentration to 7.5 mM altered evoked responses but did not replicate the injury effects to PV duration. Paired-pulse facilitation of fEPSP slopes was significantly elevated at all postinjury survivals: 1 hr, 2 days, and 7 days. These results suggest two pathological processes with differing time courses: 1) a transient impairment of presynaptic terminal functioning affecting PV durations and the transduction of afferent activity in the terminals to reliable synaptic excitation and 2) a more protracted deficit to the plasticity mechanisms underlying paired-pulse facilitation. (C) 2000 Wiley-Liss, Inc.

Original languageEnglish
Pages (from-to)370-379
Number of pages10
JournalJournal of Neuroscience Research
Volume60
Issue number3
DOIs
StatePublished - May 1 2000
Externally publishedYes

Fingerprint

Excitatory Postsynaptic Potentials
Presynaptic Terminals
Pathologic Processes
Potassium
Percussion
Hippocampal CA1 Region
Tetraethylammonium
Wounds and Injuries
Synaptic Transmission
Action Potentials
Glutamic Acid
Ions
Morbidity
Traumatic Brain Injury

Keywords

  • Hippocampus
  • Paired-pulse facilitation
  • Presynaptic volley
  • Rat
  • Traumatic brain injury

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Presynaptic excitability changes following traumatic brain injury in the rat. / Reeves, Thomas M.; Kao, Chang Q.; Phillips, Linda L.; Bullock, Ross; Povlishock, John T.

In: Journal of Neuroscience Research, Vol. 60, No. 3, 01.05.2000, p. 370-379.

Research output: Contribution to journalArticle

Reeves, Thomas M. ; Kao, Chang Q. ; Phillips, Linda L. ; Bullock, Ross ; Povlishock, John T. / Presynaptic excitability changes following traumatic brain injury in the rat. In: Journal of Neuroscience Research. 2000 ; Vol. 60, No. 3. pp. 370-379.
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