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. 2016 Oct 13;6:35220. doi: 10.1038/srep35220

Figure 4. Novel OF impairs IA-LTM persistence through a CaMK dependent mechanism.

Figure 4

(a) Schematic representation of rat brain sections at three rostrocaudal planes (AP: −3.8, −4.3, −4.8 mm, from bregma) taken from the atlas of Paxinos and Watson (1997). In stippling, the extension of the area reached by the infusions in the dorsal hippocampus (CA1). (b) Animals not exposed to OF were bilaterally infused with vehicle (Veh) or KN-93 (KN) into CA1 region of the dorsal hippocampus, 11 h after IA training as control groups. Animals exposed to a novel OF 11 h after IA training received intra CA1 infusions of either vehicle (Veh + OF 11 h) or KN-93 (KN + OF 11 h) 15 min before OF. Data are expressed as mean ± SEM of training (TR) or test session (TS) step down-latency at 7 days after IA training. *p < 0.05; **p < 0.01, ***p < 0.001, vs Veh + OF 11 h, Newman-Keuls test after ANOVA, n = 11–15 per group.