FIG. 1.

Lateral traumatic brain injury (TBI) enhanced calcineurin phosphatase activity in the hippocampus. Hippocampal tissue was isolated from adult rats at specific time points after lateral fluid percussion injury, homogenized, and subjected to an in vitro assay of calcineurin (CaN) enzymatic activity. CaN activity was measured either in the absence of stimulating cations (basal CaN activity), or in the presence of stimulating cations (maximal CaN activity). In the ipsilateral hippocampus, these experiments revealed increases in basal CaN activity at 6 h and 1 week post-TBI, relative to controls (A). Similarly, in the contralateral hippocampus, increases in basal CaN activity were detected at 6 h and 12 h post-TBI, relative to controls (B). Lateral TBI also affected the maximal activity of CaN, causing increases at 12 h post-TBI in the ipsilateral hippocampus (C), and at 6 h and 12 h post-TBI in the contralateral hippocampus (D), compared to controls. All comparisons were made by one-way analysis of variance with Dunnett's post hoc test (*p<0.05, **p<0.01).