Activities of calcineurin and phosphatase 2A in the hippocampus after transient forebrain ischemia

• Published in: Brain research 1999-05, Vol.828 (1), p.135-144
• Main Authors: Morioka, Motohiro, Fukunaga, Kohji, Hasegawa, Shu, Okamura, Akira, Korematsu, Kohjiro, Kai, Yutaka, Hamada, Jun-ichiro, Nagahiro, Shinji, Miyamoto, Eishichi, Ushio, Yukitaka
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Calcineurin; Calcineurin - analysis; Calcineurin - metabolism; Dentate Gyrus - blood supply; Dentate Gyrus - enzymology; Enzyme Activation - drug effects; Ferrous Compounds - pharmacology; Hippocampus; Immunoblotting; Immunohistochemistry; Immunosuppressive Agents - pharmacology; Ischemia; Ischemic Attack, Transient - drug therapy; Ischemic Attack, Transient - metabolism; Male; Medical sciences; Neurology; Phosphatase 2A; Phosphoprotein Phosphatases - analysis; Phosphoprotein Phosphatases - metabolism; Prosencephalon - blood supply; Prosencephalon - enzymology; Protein Phosphatase 2; Rats; Rats, Wistar; Subcellular Fractions - enzymology; Tacrolimus - pharmacology; Vascular diseases and vascular malformations of the nervous system
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/S0006-8993(99)01349-9

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.