Degradation of spectrin via calpains in the ventral horn after transient spinal cord ischemia in rabbits.

In the present study, we investigated chronological changes of mu-calpain, m-calpain and cleaved spectrin alphaII immunoreactivity in the ventral horn after transient spinal cord ischemia to investigate relationship between calpains and vulnerability to ischemia using abdominal aorta occlusion model in rabbits. Spinal cord sections at the level of L(7) were immunostained with calpains and cleaved spectrin alphaII monoclonal antibodies. mu-Calpain and m-calpain immunoreactivity was significantly increased in the ischemic ventral horn at 30 min and 1 h after ischemia/reperfusion, respectively. Thereafter, they were decreased with time after ischemia/reperfusion: at 48 h after ischemia, their immunoreactivities nearly disappeared in the ischemic ventral horn. Cleaved spectrin alphaII immunoreactivity was significantly increased in the ventral horn of spinal cord at 12 h after ischemia/reperfusion, and thereafter, its immunoreactivity was decreased with time after ischemia/reperfusion. In addition, spectrin alphaII protein level (280 kDa) was decreased from 12 h after ischemia/reperfusion; in contrast, cleaved spectrin alphaII protein level (150 kDa) was significantly increased at 12 h after ischemia/reperfusion. In conclusion, our observations in this study indicate that calpain is associated with neuronal degeneration in the ventral horn at early time after transient spinal cord ischemia via the proteolysis of spectrin alphaII.