Comparison of Phosphorylated Extracellular Signal-Regulated Kinase 1/2 Immunoreactivity in the Hippocampal Ca1 Region Induced by Transient Cerebral Ischemia Between Adult and Aged Gerbils

Abstract

In this study, the authors examined the difference of phosphorylated extracellular signal-regulated kinase 1/2 (pERK1/2) in the hippocampal CA1 region (CA1) between adult and aged gerbils after 5 min of transient cerebral ischemia. Delayed neuronal death in the CA1 of the aged group was much slower than that in the adult group after ischemia/reperfusion (I/R). pERK1/2 immunoreaction was observed in the CA1 region of the sham-operated adult gerbil. pERK1/2 immunoreactivity and protein levels in the ischemic CA1 region of the adult group were markedly increased 4 days after I/R, and then reduced up to 10 days after I/R. In contrast, pERK1/2 immunoreaction was hardly detected in the CA1 region of sham-operated aged gerbils, and the immunoreactivity increased from 1 day after the ischemic insult, and still observed until 10 days post-ischemia. In addition, pERK1/2-immunoreaction was expressed in astrocytes in the ischemic CA1 region: The expression in the ischemia-operated aged gerbils was later than that in the ischemia-operated adult gerbils. These results indicate that different patterns of ERK1/2 immunoreactivity may be associated with different processes of delayed neuronal death in adult and aged animals.

Differences in the protein expression levels of Trx2 and Prx3 in the hippocampal CA1 region between adult and aged gerbils following transient global cerebral ischemia

“…However, in the aged gerbil, numerous NeuN + neurons were found in the SP of the CA1 region 4 days after ischemia-reperfusion, with delayed neuronal death in the aged group observed 5 days after ischemia-reperfusion (data not shown). This finding was consistent with that of our previous study (27,28). …”

“…In the present study, the transient cerebral ischemia-induced delay of neuronal death was significantly slower in aged gerbils, compared with that in the adult gerbils. This result is in line with other studies and our previous studies, which reported that cerebral ischemia-induced neuronal damage in aged animals is delayed more than in adult animals due to the effects of aging on changes of lysosomes and the caspase-3-dependent apoptotic pathway in the hippocampal CA1 region (27,28,31,32). …”

“…To confirm the delayed neuronal death in the hippocampal CA1 region between the adult and aged gerbils following transient cerebral ischemia, NeuN immunohistochemistry was performed, according to the methods of the previous studies (27,28). In brief, for NeuN immunohistochemistry, the sections were sequentially treated with 0.3% hydrogen peroxide (H 2 O 2 ; Sigma-Aldrich) in PBS for 30 min and 10% normal goat serum (Vector Laboratories, Inc., Burlingame, CA, USA) in 0.05 M PBS for 30 min.…”

“…However, transient cerebral ischemia-induced neuronal damage in the hippocampal CA1 region is also affected by various factors, including the duration of ischemia/reperfusion and the age of the experimental animals (26–28). In addition, the time-dependent changes in the expression levels of Trx2 and Prx3 following cerebral ischemia remain to be fully elucidated in aged animals.…”