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. 2012 Apr 9;7(4):e34863. doi: 10.1371/journal.pone.0034863

Figure 5. Brain-specific triple deletion of mef2a, c and d impairs survival, brain size and synaptic plasticity.

Figure 5

(A) Kaplan-Meier survival curves from littermate CTL and Mef2a/c/d TKO (TKO) mice. (B) Hematoxylin and eosin staining of coronal section from littermate CTLs and Mef2a/c/d TKO. (C) Representative TUNEL staining of sections from littermate CTL and Mef2a/c/d TKO brains at 1 month of age. The white arrows indicate TUNEL stained cells. Bar graph shows an increase in apoptotic cells in Mef2a/c/d TKO mice. Data is shown as mean ± SEM. (D) Representative images of Golgi-stained CA1 pyramidal neurons from CTL and Mef2a/c/d TKO (TKO) mice (Data pooled from 15 sections/2 CTL mice and from 38 sections/4 Mef2a/c/d TKO mice). (E) CA1 LTP induction and maintenance is normal in Mef2a/c/d TKO mice (CTL, n=5; Mef2a/c/d TKO, n=6). (F) The slope of the input-output functions was significantly lower in Mef2a/c/d TKO mice compared to littermates controls (P<0.05; CTL, n=10; Mef2a/c/d TKO, n=7; solid lines indicate lines of best fit). (G) Paired-pulse facilitation is significantly increased in Mef2a/c/d TKO mice at Inter-Stimulus Interval 50, 100, 200 and 400 (mS) compared to littermate CTLs (P<0.05; CTL, n=8; Mef2a/c/d TKO, n=7).