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 larger in wild-type animals than in mice lacking the ApoE gene, whereas the facilitation in population spike amplitude after paired pulse stimulation was most pronounced in homozygous mutant mice. Primed burst stimulation induced a lasting increase in population spike amplitude of all three groups. Apart from a more pronounced initial potentiation in the homozygous mutants, primed burst potentiation was comparable in all groups. Subsequent theta burst stimulation resulted in a long-term enhanced synaptic responsiveness which was impaired in heterozygous animals. The data show that both homo- and heterozygous ApoE mutant mice display altered synaptic plasticity in the hippocampal CA1 area.