LONG-TERM POTENTIATION DEFICITS AND EXCITABILITY CHANGES FOLLOWING TRAUMATIC BRAIN INJURY

The effects of traumatic brain injury (TBI) on hippocampal long-term p otentiation (LTP) and cellular excitability were assessed at postinjur y days 2, 7, and 15. TBI was induced using a well-characterized centra l fluid-percussion model. LTP of the Schaffer collateral/commissural s ystem was assessed in vivo in urethane-anesthetized rats. Significant LTP of the population excitatory postsynaptic potential (EPSP) slope w as found only in controls, and no recovery to control levels was obser ved for any postinjury time point. Four measurement parameters reflect ing pyramidal cell discharges (population spike) indicated that TBI si gnificantly increased cellular excitability, at postinjury day 2: (1) pretetanus baseline recording showed that TBI reduced population spike threshold and latency; (2) tetanic stimulation (400 Hz) increased pop ulation spike amplitudes to a greater degree in injured animals than i n control animals; (3) tetanus-induced population spike latency shifts were greater in injured cases; and (4) tetanic stimulation elevated E PSP to spike ratios (E-S potentiation) to a greater degree in injured animals. These parameters returned to control levels, as measured on p ostinjury days 7 and 15. These results suggest that TBI induced excita bility changes persist at least through 2 days postinjury and involve a differential impairment of mechanisms subserving LTP of synaptic eff icacy and mechanisms related to action potential generation