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. Author manuscript; available in PMC: 2010 Oct 16.
Published in final edited form as: Neuron. 2008 Oct 23;60(2):353–366. doi: 10.1016/j.neuron.2008.08.027

Figure 3. Expression of αCaMKII-F89G Activity in the Tg Mice Induced Memory Deficit in One-Month Long-Term Fear Memory Tests.

Figure 3

The black bar on top column indicates the duration in which the CaMKII-F89G activity is expressed.

(A) Contextual learning in Tg mice (n = 12) during initial training was comparable to WT mice (n = 11), as shown by the similar immediate freezing response. However, a significant difference was observed in the recall test of one-month contextual fear memory in Tg mice compared to WT mice (p < 0.01).

(B) Although no significant difference was found in pretone freezing response in these mice, a significant difference in tone-elicited freezing response during recall was observed between Tg mice (n = 12) and WT mice (n = 11) (p < 0.01). All values are mean ± SEM; **p < 0.01.

(C–D) Transgenic mice with temporal expression of CaMKII-F89G restricted to learning and postlearning consolidation period performed normally in long-term memory recall tests. The black bar on the top column indicates the duration in which the CaMKII-F89G activity is expressed. The CaMKII-F89G activity in the Tg mice was selectively inhibited during the recall stage. Tg mice (n = 9) that received an i.p. injection of NM-PP1 (16.6 ng/g) 15 min prior the recall tests exhibited normal retrieval in comparison to that of wild-type mice (n = 11) in one-month contextual fear conditioning (C) and cued fear conditioning tests (D). All values are mean ± SEM.