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. 2012 Jul 25;32(30):10423–10437. doi: 10.1523/JNEUROSCI.5491-11.2012

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Copyright © 2012 the authors 0270-6474/12/3210423-15$15.00/0

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Figure 6. — GGA1 is depleted in the acute phase after TBI. A, Western blot analysis of GGA3 and GGA1 levels in Gga3^+/+, Gga3^+/−, and Gga3^−/− mice 48 h after injury. B, The graph represents GGA3 levels normalized to GAPDH (mean ± SEM of 8 Gga3^+/+, 5 Gga3^+/−) and expressed as arbitrary units. GGA3 levels are reduced by 55% (p = 0.002) in the injured hemisphere of Gga3^+/+ mice and 48% (p = 0.0184) in the injured hemisphere of Gga3^+/− mice at 48 h after injury. ^#GGA3 levels are reduced 59% (p = 0.0019) in the injured hemisphere of Gga3^+/− mice compared with Gga3^+/+ mice. *GGA3 levels are reduced 53% (p = 0.0002) in the contralateral hemisphere of Gga3^+/− mice compared with Gga3^+/+ mice. C, The graph represents GGA1 levels normalized to GAPDH (mean ± SEM of 10 Gga3^+/+, 5 Gga3^+/− and 8 GGA3^−/−) and expressed as arbitrary units. GGA1 levels are reduced by 67% (p < 0.001) in the injured hemisphere of GGA3^+/+ mice, by 53% (p = 0.0019) in the injured hemisphere of GGA3^+/− mice, and by 61% (p < 0.0001) in the injured hemisphere of Gga3^−/− mice 48 h after injury. Statistical analysis of data was performed using a paired t test.