TFEB activation and translocation to the nucleus is reduced by A2AR activation after TBI. A, Western blot analysis of TFEB levels in ipsilateral retrosplenial cortex tissue lysates (nucleus and cytoplasm) obtained from mice in the sham, WT + TBI and KO + TBI groups. B, TFEB nuclear content as x % of total (nuclear and cytoplasmic) signal. Histone 2B and β‐actin were used as nuclear and cytoplasmic purity controls, n = 5, KO + TBI group vs WT + TBI group, **P < 0.01. C, Western blot analysis of PGC‐1α levels in ipsilateral retrosplenial cortex tissue lysates (nucleus and cytoplasm) obtained from mice in the sham, WT + TBI and KO + TBI groups. D, PGC‐1α nuclear content as x % of total (nuclear and cytoplasmic) signal. Histone 2B and β‐actin were used as nuclear and cytoplasmic purity controls, n = 5, KO + TBI group vs WT + TBI group, **P < 0.01. E, Western blot analysis of the protein level of p‐TFEB in RSC tissue lysates obtained from sham and TBI mice 1 d after injury. F, The p‐TFEB levels shown in (E) were quantified and normalized to β‐actin. Data are presented as the means ± SDs, n = 6, KO + TBI group vs WT + TBI group, **P < 0.01. KO, knockout; RSC, retrosplenial cortex; TBI, traumatic brain injury; TFEB, transcription factor EB; WT, wild‐type