Neuronal damage is much delayed and microgliosis is more severe in the aged hippocampus induced by transient cerebral ischemia compared to the adult hippocampus

Activation of astrocytes and microglia in the post-ischemic hippocampus has been investigated using ischemia models. The aim of this study was to investigate differences of delayed neuronal death and gliosis in the hippocampal CA1 region (CA1) between adult and aged gerbils. Delayed neuronal death in the CA1 was later in the aged gerbil than in the adult gerbil after ischemia/reperfusion (I/R). GFAP-immunoreactive (+) astrocytes and Iba-1+ microglia were activated following neuronal damage in both adult and aged gerbils after I/R. Changes in GFAP immunoreactivity and protein levels were similar in both groups: they were distinctly increased from 3 days after I/R. Iba-1 immunoreactivity and protein levels in the aged sham gerbil were much higher than those in the adult sham gerbil. Activation of microglia in the CA1 of the aged group was slower, lower 4 days and much higher 7 days than that in the adult gerbil after I/R. These observations indicate that delayed neuronal death in the CA1 of the aged group is slower than that in the adult group after I/R. In addition, microglial activation, not astrocytes, in the aged ischemia group is slower and more intense than that in the adult ischemia group.