MICE DEFICIENT FOR PRION PROTEIN EXHIBIT NORMAL NEURONAL EXCITABILITYAND SYNAPTIC TRANSMISSION IN THE HIPPOCAMPUS

We recorded in the CA1 region from hippocampal slices of prion protein (PrP) gene knockout mice to investigate whether the loss of the norma l form of prion protein (PrPC) affects neuronal excitability as well a s synaptic transmission in the central nervous system. No deficit in s ynaptic inhibition was found using field potential recordings because (i) responses induced hy stimulation in stratum radiatum consisted of a single population spike in PrP gene knockout mice similar to that re corded from control mice and (ii) the plot of field excitatory postsyn aptic potential slope versus the population spike amplitude showed no difference between the two groups of mice. Intracellular recordings al so failed to detect any difference in cell excitability and the revers al potential for inhibitory postsynaptic potentials. Analysis of the k inetics of inhibitory postsynaptic current revealed no modification. F inally, we examined whether synaptic plasticity was altered and found no difference in long-term potentiation between control and PrP gene k nockout mice. On the basis of our findings, we propose that the loss o f the normal form of prion protein does not alter the physiology of th e CA1 region of the hippocampus.