THE EFFECT OF COMBINED FLUID PERCUSSION AND ENTORHINAL CORTICAL-LESIONS ON LONG-TERM POTENTIATION

Among the pathological processes initiated by traumatic brain injury a re excessive neuroexcitation and target cell deafferentation. The curr ent study examines the contribution of these injury components, separa tely as well as their combined effect, on postinjury alterations in th e capacity for long-term potentiation and the immunolocalization of N- methyl-D-aspartate receptors and GABA. Adult rats underwent central fl uid percussion traumatic brain injury, electrolytic bilateral entorhin al cortex lesions, or a combined injury of both procedures separated b y 24 h. At two or 15 days postinjury, the capacity for long-term poten tiation of the Schaffer collateral-commissural input to CA1 was measur ed in acute electrophysiological recordings. Entorhinal cortical lesio ns resulted in time-dependent increases in the effectiveness of tetani c stimulation to elevate population postsynaptic potentials and popula tion spike amplitudes. These lesions also resulted in a marked intensi fication in the density of iv-methyl-D-aspartate receptors in the CA1 stratum lacunosum-moleculare. All injury conditions that included flui d percussion as a component (alone or in combined injuries) produced a persistent impairment in long-term potentiation of the evoked populat ion postsynaptic potentials. Thus, in combined injuries, the presence of concussion-induced neuroexcitation attenuated deafferentation-induc ed response increases. Both N-methyl-D-aspartate receptor and GABA imm unobinding following combined injuries were also reduced relative to t hose observed following entorhinal lesions alone. The present results suggest that a process of receptor plasticity, possibly involving reac tive synaptogenesis, may contribute to postdeafferentation enhancement s of long-term potentiation, and that a traumatic brain insult will at tenuate these enhancements. This interaction of different injury compo nents suggests that recovery of function following brain injury may be enhanced by pharmacological reduction of neuroexcitation during posti njury intervals of reactive receptor plasticity. (C) 1997 IBRO.