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. 2017 May;24(5):199–209. doi: 10.1101/lm.044602.116

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© 2017 Vogel Ciernia et al.; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first 12 months after the full-issue publication date (see http://learnmem.cshlp.org/site/misc/terms.xhtml). After 12 months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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Figure 5. — BAF53bΔSB2 transgenic mice have intact short-term and impaired long-term memory. (A) Mice received 10 min training in an environment with two identical objects and received a retention test either 90 min (short-term) or 24 h (long-term) later in which one object is moved to a new location (OLM). (B) Wild-type (n = 22), BAF53bΔSB2^low (n = 10), and BAF53bΔSB2^high mutant mice (n = 13) all exhibit similar 90-min short-term hippocampus-dependent OLM (ANOVA F_(2,42) = 0.60, P = 0.55). All three genotypes showed a DI significantly different from zero (wild-type t-test t₍₂₁₎ = 11.54, P < 0.0001; BAF53bΔSB2^low t-test t₍₉₎ = 8.31, P < 0.0001 and BAF53bΔSB2^high t-test t₍₁₂₎ = 9.80, P < 0.0001) (C) BAF53bΔSB2^low (n = 12) and BAF53bΔSB2^high mutant mice (n = 9) show significant deficits in 24-h long-term OLM compared with wild-type littermates (n = 21) (ANOVA F_(2,39) = 30.37, P < 0.0001, Bonferroni corrected t-test: BAF53bΔSB2^low versus wild type t₍₃₁₎ = 5.81, P < 0.05; BAF53bΔSB2^high versus wild type t₍₂₈₎ = 6.82, P < 0.05). (D) Mice received 10-min training in an environment with two identical objects and received a retention test 90 min (short-term) or 24 h (long-term) later in which one object is replaced with a novel one. (E) In a hippocampus-independent object recognition task BAF53bΔSB2^low (n = 9) and BAF53bΔSB2^high (n = 8) exhibit 90-min short-term ORM similar to wild-type littermates (n = 21) (Kruskal–Wallis H_(2,35) = 2.19, P = 0.33). All three genotypes showed a DI significantly different from zero (wild-type t-test t₍₂₀₎ = 13.14, P < 0.0001; BAF53bΔSB2^low t-test t₍₈₎ = 10.53, P < 0.0001 and BAF53bΔSB2^high t-test t₍₇₎ = 9.01, P < 0.0001). (F) BAF53bΔSB2^low (n = 10) and BAF53bΔSB2^high mutant mice (n = 11) show significant deficits in 24 h long-term ORM compared with wild-type littermates (n = 17) (ANOVA F_(2,35) = 15.93, P < 0.0001, Bonferroni corrected t-test: BAF53bΔSB2^low versus wild type t₍₂₅₎ = 4.26, P < 0.05; BAF53bΔSB2^high versus wild type t₍₂₆₎ = 5.05, P < 0.05). (G) AAV-cofilinS3D is expressed throughout dorsal hippocampus of wild-type and BAF53bΔSB2^high mutant mice. Viral expression is localized by HA tag. Scale bar 200 µm. (H) BAF53bΔSB2^high mice with AAV-GFP viral expression in dorsal hippocampus (n = 13) show impaired OLM compared with wild-type littermates with hippocampal AAV-GFP expression (n = 14) (ANOVA no main effect for genotype F_(1,57) = 2.01, P = 0.16, no effect of virus F_(1,57) = 4.00, P = 0.05 but a significant interaction F_(1,57) = 4.57, P = 0.04). Overexpression of AAV-cofilinS3D in dorsal hippocampus of BAF53bΔSB2^high mice (n = 18) completely restored the long-term memory formation compared with wild-type littermates with AAV-cofilinS3D expression (n = 16) (Bonferroni corrected t-test: AAV-GFP and BAF53bΔSB2^high mice with AAV-GFP t₍₂₅₎ = 2.38, P < 0.05; wild-type AAV-cofilinS3D and BAF53bΔSB2^high mice with AAV-cofilinS3D t₍₃₂₎ = 0.54, P > 0.05). Mean (±SEM).