tacrolimus and ferrous-chloride

We investigated the changes in the enzyme activity and immunoreactivity of calcineurin in the rat hippocampus after transient forebrain ischemia. Immediately after 20-min transient forebrain ischemia, calcineurin activity decreased to about 40% of the control in the CA1 region and to about 55% in other regions. Protein phosphatase 2A activity showed no remarkable changes. By 12 h after ischemia, calcineurin activity recovered, more in the CA1 region than in other regions. At 24 h it decreased again, but only in the CA1 region. Immunohistochemical- and immunoblot analyses showed no remarkable change in calcineurin in any region of the hippocampus within 12 h after ischemia. Thus, the activity of calcineurin is dissociated from its immunoreactivity and quantity. Several studies have suggested that unknown inhibitory factor(s) and/or reversible changes in calcineurin act to modify enzyme activity after ischemia. In contrast, phosphatase 2A activity underwent no obvious changes during the post-ischemia period we examined. This unique time course of calcineurin activity may contribute to the mechanism of ischemic neuronal injury.

Topics: Animals; Calcineurin; Dentate Gyrus; Enzyme Activation; Ferrous Compounds; Immunoblotting; Immunohistochemistry; Immunosuppressive Agents; Ischemic Attack, Transient; Male; Phosphoprotein Phosphatases; Prosencephalon; Protein Phosphatase 2; Rats; Rats, Wistar; Subcellular Fractions; Tacrolimus