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Fig. 6 | Molecular Brain

Fig. 6

From: Pre- and post-synaptic roles for DCC in memory consolidation in the adult mouse hippocampus

Fig. 6

Deletion of DCC from CA3 pyramidal neurons, but not CA1 pyramidal neurons, impairs HFS-induced LTP in the adult hippocampus. a-b Representative evoked AMPAR-mediated EPSCs (a) and group data (b) recorded at − 70 mV in response to Schaffer collateral stimulation from control littermates (left, black) and R4ag11-Cre/DCCfl/fl (CA1 cKO; right, red) prior to and following (20 min post-HFS) brief high-frequency stimulation (1 s at 100 Hz). The amplitude of EPSCs remained significantly potentiated after 25 min in slices from both R4ag11-Cre/DCCfl/fl (144 ± 10% of baseline, p < 0.001) and controls (140 ± 12% of baseline, p = 0.02) compared to baseline values (Main effect of HFS: F1,18 = 20.78, p < 0.001; Interaction genotype X HFS: F1,18 = 0.20, p = 0.659). c Paired-pulse ratio (50 ms ISI) was not significantly changed between R4ag11-Cre/DCCfl/fl (CA1 cKO) mice and control littermates (p = 0.602). d-f Representative evoked AMPAR-mediated EPSCs (d) and group data (e) recorded at − 70 mV in response to Schaffer collateral stimulation from control littermates (left, black) and Grik4-Cre/DCCfl/fl (CA3 cKO; right, green) prior to and following (20 min post-HFS) brief high-frequency stimulation (1 s at 100 Hz). AMPAR-mediated EPSCs were not significantly different from baseline values (113 ± 6% of baseline values, p = 0.913) compared to controls (145 ± 9% of baseline, p = 0.002) (Interaction for genotype X HFS: F1,14 = 6.30, p = 0.025), with no appreciable change in the paired-pulse ratio (f; Interaction for genotype X HFS: p = 0.780). ** denotes p < 0.01

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