FIG. 2.

Lateral traumatic brain injury (TBI) enhanced calcineurin phosphatase activity in the neocortex. Neocortical 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 (basal CaN activity) or presence (maximal CaN activity) of stimulating cations. In the ipsilateral neocortex, basal CaN activity increased significantly above control levels by 1 week and 2 weeks post-TBI (A). The contralateral neocortex also showed an increase in basal CaN activity, but weeks later, at 4 weeks post-TBI, compared to controls (B). The maximal activity of CaN also changed after lateral TBI, increasing significantly over control levels at 1 week and 2 weeks post-TBI in the ipsilateral neocortex (C), and at 4 weeks post-TBI in the contralateral neocortex (D). All comparisons were made by one-way analysis of variance with Dunnett's post-hoc test (*p<0.05, **p<0.01).