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. 2009 Apr 1;29(13):4218–4227. doi: 10.1523/JNEUROSCI.4225-08.2009

Figure 3.

Figure 3.

BLA-specific deletion of Mecp2 results in elevated anxiety-like behavior with normal locomotion and motor coordination. A, AAV-CreGFP mice displayed motor coordination indistinguishable from that of AAV-GFP-injected mice on the rotarod test through eight trials. B, Locomotor activity was assessed by consecutive horizontal beam breaks for a 60 min testing period in 5 min increments. Inset, Total numbers of beam breaks during the test period were similar between AAV-GFP- and AAV-CreGFP-injected mice. C, D, Localized knockdown of Mecp2 in the BLA resulted in heightened anxiety-like behavior. In the elevated-plus maze test, the localized deletion of Mecp2 in the BLA resulted in a significant increase in the time spent in the closed arm (p < 0.05) (C) as well as a significant increase in the latency to enter the open arm (p < 0.05) (D), indicating an increase in anxiety-related behavior. E–H, BLA-specific Mecp2 knockdown mice were assessed for the open-field test. Presented are time in center field (E), duration ratio of time spent in complete center field to that to periphery (F), latency to enter to center field (G), and frequency to enter center field (H). Localized knockdown of Mecp2 in BLA resulted in a significant decrease in duration ratio and a significant increase in latency to enter the center field compared with AAV-GFP mice (p < 0.05), further supporting an increase in anxiety-related behavior. *p < 0.05 by Student's t test; AAV-GFP, n = 13; AAV-CreGFP, n = 10 for A–H.