(A) Paired pulses evoked by stimulation of the Schaffer collaterals in slices from P30–45 mice in normal artificial cerebrospinal fluid (aCSF)

(B) Quantification of the number of population spikes in WT and PrP-null slices in aCSF. (C, top) Minimum stimulus intensity required to evoke a single population spike in WT and PrP-null slices. (middle) Stimulus intensity required to evoke maximum single population spike amplitude. (bottom) Extent of paired pulse facilitation in WT and PrP-null slices. (D, top) Field potentials recorded from PrP-null slices before and after the application of 50 μM APV as shown for P2. (bottom) Quantification of the number of population spikes before and after APV application in PrP-null slices. (E) Evoked field potentials recorded after 5 min of perfusion in zero-magnesium aCSF (ZM-aCSF). The gray arrows indicate successive population spikes, which are augmented in the PrP-null slices. (F, left) The number of population spikes overriding the fEPSP in slices exposed to ZM-aCSF. (second graph) Time to the observance of the first seizurelike discharge in ZM-aCSF. (third graph) Time to the occurrence of the first seizurelike event (SLE) upon perfusion with ZM-aCSF. (right) Duration of seizurelike events in WT and PrP-null slices. The black and gray arrowheads indicate the primary population spikes and the additional population spikes, respectively, overriding the fEPSP in each pulse (P1 and P2); these latter polyspikes were only observed in PrP-null mice. Data are represented as mean ± SEM (error bars) with statistical significance denoted as *, P < 0.05 and **, P < 0.001. Numbers in parentheses indicate the number of slices.<p><b>Copyright information:</b></p><p>Taken from "Prion protein attenuates excitotoxicity by inhibiting NMDA receptors"</p><p></p><p>The Journal of Cell Biology 2008;181(3):551-565.</p><p>Published online 5 May 2008</p><p>PMCID:PMC2364707.</p><p>