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. 2021 Mar 15;9:tkaa050. doi: 10.1093/burnst/tkaa050

Figure 6.

Figure 6.

Neuronal dysfunction in hippocampus mediated by brain edema after TBI. (a, b, c) Compared with the sham group, CREB and pCREB (ser133) were at their lowest levels at 72 h post TBI (p < 0.01). (a, d) Compared with the sham group, GCN2 level increased significantly from 3 h to 15 d after TBI (p < 0.01). (e, f) Escape latency and search time in the MWM test: compared with the sham group, there were no significant differences in the results of pre-injury t-tests (p > 0.05) and significant difference in behavioral tests performed in the time points of 11, 13 and 15 d after TBI (p < 0.01) (**p < 0.01). TBI traumatic brain injury, CREB cAMP response element binding protein, d day(s), GAPDH glyceraldehyde-3-phosphate dehydrogenase, GCN2 general control nonrepressed 2