SELECTIVE LOSS OF HIPPOCAMPAL LONG-TERM POTENTIATION, BUT NOT DEPRESSION, FOLLOWING FLUID PERCUSSION INJURY

We investigated the early effects of in vivo fluid percussion injury ( FPI) on hippocampal synaptic potentials and excitability. In vitro fie ld potential recordings and immunocytochemistry were performed in the CA1 region in slices from naive, post-FPI, or sham-operated rats. The following electrophysiological and morphological parameters were affec ted following FPI: (1) threshold for population spike generation was i ncreased suggesting that post-FPI neurons were hypoexcitable; (2) long -term potentiation (LTP) could not be induced in injured hippocampi; ( 3) GFAP and inducible NO synthase (iNOS) immunoreactivity were enhance d post-FPI; and (4) following injury, synaptophysin immunoreactivity w as enhanced in CAI stratum radiatum. The effects of FPI on synaptic pl asticity were LTP-specific, since long-term depression (LTD) could be equally induced and maintained in post-FPI, sham-operated and control slices. Sham-operated slices were characterized by synaptic excitabili ty indistinguishable from naive controls, but displayed decreased abil ity for LTP production and expressed high levels of iNOS. We conclude that FPI causes a selective loss of LTP, possibly due to a previous po tentiation induced by trauma as reflected by the increased expression of synaptic proteins. Sham surgical procedures were, however, not with out effects on long-term potentiation itself; the latter effects appea r to be mediated by an increased production of NO. Our study demonstra tes for the first time that hippocampal slices can be used to investig ate the correlates of in vivo FPI. Furthermore, we describe LTP-specif ic deficits in post-traumatic brain injury, suggesting that FPI can se lectively erase one of the two main NMDA-dependent forms of synaptic p lasticity in the hippocampus. (C) 1998 Elsevier Science B.V.