I. Veinbergs et al., ALTERED LONG-TERM POTENTIATION IN THE HIPPOCAMPUS OF APOLIPOPROTEIN E-DEFICIENT MICE, Neuroscience letters, 249(2-3), 1998, pp. 71-74
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.