Skip to main content
. Author manuscript; available in PMC: 2015 Nov 1.
Published in final edited form as: Neurobiol Learn Mem. 2014 Jun 14;0:30–37. doi: 10.1016/j.nlm.2014.06.005

Fig. 4.

Fig. 4

Dissociable effects of Dnmt1 and Dnmt3a CKO on LTP in hippocampal CA1. (A–B) Hippocampal slices prepared from Dnmt1 CKO mice (n=10) had normal theta burst-induced LTP relative to CTL (n=9), however Dnmt3a CKO slices had deficits in LTP following theta burst (time × genotype interaction F(159, 3517) = 4.006, p < 0.001, 90.0 % of points after theta burst p ≤ 0.05). (C) Dnmt3a CKO mice were also impaired following high-frequency stimulation (time × genotype interaction F(427, 6213) = 3.392, p < 0.001, 68.77% of points after high frequency stimulation p ≤ 0.05; 100% of points significant 157 minutes after LTP induction until end of recording) relative to CTL (Dnmt3a CKO, theta burst n=10, HFS n=6; CTL, theta burst n=12, HFS n=7). θ = theta burst; ↑= high frequency stimulation. Insets (A–C) - Representative traces from CTL and Dnmt1 or Dnmt3a CKO slices 30 (A, B) or 120 minutes (C) after LTP induction. Black traces = baseline, gray (CTL), or colored traces are after LTP induction. (D, E) Input-output relationships were normal in both Dnmt1 (n=11) and Dnmt3a (n=6) CKOs relative to control littermate (CTL, n=9, 8) hippocampal slices. (F, G) Dnmt1 (n=10) CKOs exhibited significantly enhanced paired pulse ratio at 30 ms interstimulus interval (t(15) = 2.346, p = 0.033), suggesting decreased neurotransmitter release probability compared with CTL (n=7). Dnmt3a (n=6) CKO mice had paired pulse ratios that did not differ from CTL (n=8). *p ≤ 0.05 vs. CTL.