The Effect of Cortical Cold Injury on Calbindin Immunoreactivity in the Mouse Brain

• Main Authors: Sheng-Huang Lin, 林聖皇
• Other Authors: 邱鐵雄
• Format: Others
• Language: en_US
• Published: 2000
• Online Access: http://ndltd.ncl.edu.tw/handle/58304547280233153341

碩士 === 慈濟醫學院 === 醫學研究所 === 88 === Abstract Excessive intracellular calcium is one of the major mechanisms, which cause necrotic death or apoptosis of neural cells. Different forms of injury including hypoglycemia, seizure, and hypoxia-ischemia can cause such calcium overload and neuronal damage. Calbindin, an intracellular calcium binding protein, exerts its effect by buffering excessive Ca2+ and protects the neural cell against calcium overload. Here we used cortical cold injury model in mice to examine its effect on the expression of calbindin immunoreactivity. The result reveals that cold-induced injury decreased the immunoreactivity of calbindin at the core and adjacent area of the injury lasting for about three days. Recovery of calbindin expression was observed on the fifth and seventh day after cold injury. This result suggests that calcium overload may participate in the pathogenesis of cortical cold injury. We also investigated the expression of CD 11b (Mac-1) on the acute stage of cortical cold injury (the first day after cold injury). Many CD 11b positive cells were found in the core and adjacent area. This result indicates that inflammation may play an important role in causing cortical cold injury.