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. Author manuscript; available in PMC: 2013 Jan 8.
Published in final edited form as: Mol Cell Neurosci. 2011 May 24;47(4):293–305. doi: 10.1016/j.mcn.2011.05.008

Fig. 4. Synaptic plasticity in CA1.

Fig. 4

(A) SC-CA1 LTP induced by two trains at 100 Hz was significantly reduced in Df(16)A+/− mice After 1 hr WT fEPSPs were potentiated by 63.12% (n = 9) and Df(16)A+/− responses by 29.77% (n = 8, p = 0.001). (B) SC-CA1 LTP induced by a theta burst protocol did not differ between genotypes. After 1 hr potentiation was 62.5 ± 10.5% in WT (n = 7) and 55.0 ± 5.3% in Df(16)A+/− (n = 9, p = 0.50). (C) SC-CA1 L-LTP induced by three applications of a 200 Hz based protocol did not differ between genotypes. After 2.5 hrs potentiation was 61.7 ± 7.3% in WT (n = 7) and 64.4 ± 13.6% in Df(16)A+/− (n = 7, p = 0.86). (D) TA-CA1 LTP induced by two trains at 100 Hz stimulation was similar in WT and Df(16)A+/− mice. After 1 hr potentiation was 61.7 ± 7.3% in WT (n = 7) and 64.4 ± 13.6% in Df(16)A+/− (n = 7, p = 0.86). (E) SC-CA1 LTD induced by 1 Hz stimulation for 15 min was comparable in the two genotypes. After 1 hr depression was 27.2 ± 2.8% in WT (n = 13) and 31.3.0 ± 3.0% in Df(16)A+/− (n = 18, p = 0.34). (F) SC-CA1 depotentiation induced by 1 Hz stimulation for 15 min after LTP induction by 2 × 100 Hz trains was not different between genotypes. After 1 hr depotentiation was 23.5 ± 5.6% in WT (n = 5) and 23.1 ± 3.6% in Df(16)A+/− (n = 8, p = 0.96).