Mice deficient for prion protein exhibit normal neuronal excitability and synaptic transmission in the hippocampus

摘要

We recorded in the CA1 region from hip- pocampal slices of prion protein (PrP) gene knockout mice to investigate whether the loss of the normal form of prion protein (PrP~C) affects neuronal excitability as well as synaptic transmission in the central nervous system. No deficit in synaptic inhibition was found using field potential recordings because (i) responses induced by stimulation in stratum radiatum consisted of a single population spike in PrP gene knockout mice similar to that recorded from control mice and (ii) the plot of field excitatory postsynaptic potential slope versus the population spike amplitude showed no difference between the two groups of mice.