ALTERED SYNAPTIC PLASTICITY IN HIPPOCAMPAL CA1 AREA OF APOLIPOPROTEIN-E DEFICIENT MICE

IN mice with a homozygous or heterozygous deficiency for ApoE as well as in wild-type animals we established synaptic responsiveness in the hippocampal CA1 area following stimulation of the SchafFer/commissural fibers. The maximal population spike amplitude was significantly larg er in wild-type animals than in mice lacking the ApoE gene, whereas th e facilitation in population spike amplitude after paired pulse stimul ation was most pronounced in homozygous mutant mice. Primed burst stim ulation induced a lasting increase in population spike amplitude of al l three groups. Apart from a more pronounced initial potentiation in t he homozygous mutants, primed burst potentiation was comparable in all groups. Subsequent theta burst stimulation resulted in a long-term en hanced synaptic responsiveness which was impaired in heterozygous anim als. The data show that both home- and heterozygous ApoE mutant mice d isplay altered synaptic plasticity in the hippocampal CA1 area.