AlphaII-spectrin breakdown product increases in principal cells in the gerbil main olfactory bulb following transient ischemia.

In pathological states, calpains in neurons easily degrade spectrin and yield specific fragments called spectrin breakdown products characterized by their high stabilities both in vitro and in vivo. In the present study, we investigated chronological changes in alphaII-spectrin immunoreactivity and protein levels using the antibody to detect both the naïve form and breakdown products of alphaII-spectrin in the gerbil main olfactory bulb (MOB) after 5 min of transient forebrain ischemia. In sham-operated gerbils, weak alphaII-spectrin immunoreactivity was detected in principal (mitral and tufted) cells. Ten days after ischemia/reperfusion, alphaII-spectrin immunoreactivity was increased in principal cells. Fifteen days after ischemia/reperfusion, alphaII-spectrin immunoreactivity in the somata and processes of principal cells was markedly increased. Thereafter, alphaII-spectrin immunoreactivity in the principal cells in the ischemic MOB was decreased with time. In Western blot study, spectrin protein bands were detected in naïve form (230 kDa) and its breakdown product (150 kDa). The breakdown product in MOB homogenates were significantly increased 15 days after ischemia/reperfusion and thereafter decreased with time after ischemia/reperfusion. Our results indicate that alphaII-spectrin breakdown product in the gerbil MOB is changed in principal cells after ischemic insult.