Fig. 3
Expression of sAPPα partially restored hippocampal LTP in transgenic mice. a, b There were no significant genotype or treatment effects on the I/O curves in CA1 for either the (a) EPSP slope, (p = 0.17 and 0.14, respectively) or (b) population spike amplitude (p = 0.14 and 0.63, respectively, indicating that basal synaptic transmission and cell excitability were unaffected in Tg mice and sAPPα over-expression. c There were no group differences in paired-pulse facilitation of the fEPSP (WT-control: n = 22; Tg-control: n = 12; Tg-sAPPα: n = 17, F(2,48) = 0.32, p = 0.73), nor a group x interval interaction (F(2,48) = 0.96, p = 0.39), indicating no difference in basal transmitter release probability. (d) Paired-pulse inhibition was reduced in Tg-controls compared to WT-controls (WT-control: n = 16; Tg-control: n = 10; F(2,38) = 4.18, p = 0.023), indicating an impairment of recurrent inhibition. A partial rescue was produced by sAPPα expression. (e, f) TBS delivered to the Schaffer collaterals induced robust potentiation in all groups but which decayed at different rates between groups. Significant group differences were observed at both 1 h (F(2,49) = 4.20, p = 0.021) and 2 h post-TBS (F(2,49) = 5.44, p = 0.007) with Tg-controls significantly impaired (26.1 ± 6.9%, n = 11) compared to WT-controls (51.9 ± 7.4%, n = 21; p < 0.05) after 1 h. LTP in the Tg-sAPPα indicating a partial recovery of LTP expression. The partial recovery was still observed 2 h post-TBS (WT-controls: 36.8 ± 7.5%, n = 21; Tg-controls: 9.7 ± 6.2%, n = 11; Tg-sAPPα: 22.5 ± 3.5%, n = 18). *p < 0.05