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. 2009 Aug 10;4(8):e6574. doi: 10.1371/journal.pone.0006574

Figure 6. Dp71 loss alters synaptic transmission and plasticity in CA1 hippocampal area.

Figure 6

KO: Filled symbols; WT: Open symbols. A. Basal glutamatergic transmission mediated via AMPAr. Sample traces (Top) show examples of AMPAr-mediated fEPSPs in response to single pulses (stimulation intensity: 300 µA); neurotransmission (bottom) is expressed as AMPAr-mediated fEPSP slopes plotted against presynaptic fiber volley (PFV) slopes (PFV-fEPSP coupling). B. NMDAr component of glutamatergic transmission. Sample traces of NMDAr-mediated fEPSPs (Top, stimulation intensity: 500 µA) and NMDAr-mediated PFV-fEPSP coupling (bottom). The fEPSPs were isolated in the presence of bicuculline and DNQX. C–D. Time-course of LTP induced by HFS (time 0) at 2×50 Hz (C) and 2×100 Hz (D). Synaptic strength is expressed as percent change of fEPSP slopes from baseline taken as 100% (dotted line) and plotted against time. Sample traces show averaged fEPSPs recorded in response to constant test stimuli in stratum radiatum of CA1 area before (a) and 45–60 min after induction (b). E. PPF induced by stimulus pairs (50 ms inter-pulse interval) and expressed as the ratio of the second over the first fEPSP slopes. *p<0.02.F. Time course of LTD of the fEPSP after low frequency stimulation (900 pulses at 1 Hz). Sample traces show averaged fEPSPs recorded before (a) and 60 min after induction (b) (scale bars: 5 ms, 0.5 mV).