Neuronal damage and gliosis in the somatosensory cortex induced by various durations of transient cerebral ischemia in gerbils

Abstract Although many studies regarding ischemic brain damage in the gerbil have been reported, studies on neuronal damage according to various durations of ischemia–reperfusion (I–R) have been limited. In this study, we examined neuronal damage/death and glial changes in the somatosensory cortex 4 days after 5, 10 and 15 min of transient cerebral ischemia using the gerbil. To examine neuronal damage, we used Fluoro-Jade B (F-J B, a marker for neuronal degeneration) histofluorescence staining as well as cresyl violet (CV) staining and neuronal nuclei (NeuN, neuronal marker) immunohistochemistry. In the somatosensory cortex, some CV and NeuN positive (+ ) neurons were slightly decreased only in layers III and VI in the 5 min ischemia-group, and the number of CV+ and NeuN+ neurons were decreased with longer ischemic time. The F-J B histofluorescence staining showed a clear neuronal damage in layers III and VI, and the number of F-J B+ neurons was increased with time of ischemia–reperfusion: in the 15 min ischemia-group, the number of F-J B+ neurons was much higher in layer III than in layer VI. In addition, we immunohistochemically examined gliosis of astrocytes and microglia using anti-glial fibrillary acidic protein (GFAP) and anti-ionized calcium-binding adapter molecule 1 (Iba-1) antibody, respectively. In the 5 min ischemia-group, GFAP+ astrocytes and Iba-1+ microglia were distinctively increased in number, and their immunoreactivity was stronger than that in the sham-group. In the 10 and 15 min ischemia-groups, numbers of GFAP+ and Iba-1+ glial cells were much more increased with time of ischemia–reperfusion; in the 15 min ischemia-group, their distribution patterns of GFAP+ and Iba-1+ glial cells were similar to those in the 10 min ischemia-group. Our fining indicates that neuronal death/damage and gliosis of astrocytes and microglia were apparently increased with longer time of ischemia–reperfusion.