ALTERED LONG-TERM POTENTIATION IN THE HIPPOCAMPUS OF APOLIPOPROTEIN E-DEFICIENT MICE

Recent studies suggest that apolipoprotein E (apoE) plays a neurotroph ic role in the central nervous system and that an aberrant function of this molecule might result in neurodegeneration. Supporting this noti on, apoE-deficient mice show neurodegenerative and cognitive alteratio ns. To characterize physiological changes associated with synaptic dam age and cognitive impairment in apoE-deficient mice, we investigated s ynaptic plasticity in the hippocampus of urethane anesthetized mice. E lectrical stimulation was delivered to the perforant pathway and the r esulting evoked field excitatory postsynaptic potential (EPSP) and pop ulation spike were recorded in the hilus. Long-term potentiation, as m easured in the population spike, was reduced by 50% in apoE-deficient mice when compared to wild-type controls. In contrast, there were no s ignificant differences in the evoked field EPSP between wild-type and apoE-deficient mice following high-frequency stimulation. These result s support the notion that cognitive impairment and synaptic loss in th e hippocampus of apoE-deficient mice might be associated with impaired long-term potentiation. (C) 1998 Elsevier Science Ireland Ltd. All ri ghts reserved.