| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 1913266 | Journal of the Neurological Sciences | 2015 | 8 Pages |
•NHE1 immunoreactivity alters in pyramidal neurons of hippocampal CA1 after ischemic insult.•NHE1 is newly expressed in astrocytes in CA1 after ischemic insult.•IPC protects CA1 pyramidal neurons from ischemic damage.•IPC attenuates NHE1 immunoreactivity in CA1 pyramidal neurons after ischemic injury.
The participation of Na+/H+ exchanger (NHE) in neuronal damage/death in the hippocampal CA1 region (CA1) induced by transient forebrain ischemia has not been well established, although acidosis may be involved in neuronal damage/death. In the present study, we examined the effect of ischemic preconditioning (IPC) on NHE1 immunoreactivity following a 5 min of transient forebrain ischemia in gerbils. The animals used in the study were randomly assigned to four groups (sham-operated-group, ischemia-operated-group, IPC plus (+) sham-operated-group and IPC + ischemia-operated-group). IPC was induced by subjecting animals to 2 min of ischemia followed by 1 day of recovery. A significant neuronal loss was found in the stratum pyramidale (SP) of the CA1, not the CA2/3, of the ischemia-operated-group at 5 days post-ischemia. However, in the IPC + ischemia-operated-group, neurons in the SP of the CA1 were well protected. NHE1 immunoreactivity was not detected in any regions of the CA1-3 of the sham- and IPC + sham-operated-groups. However, the immunoreactivity was apparently expressed in the SP of the CA1-3 after ischemia, and the NHE1immunoreactivity was very weak 5 days after ischemia; however, at this point in time, strong NHE1immunoreactivity was found in astrocytes in the CA1. In the CA2/3, NHE1immunoreactivity was slightly changed, although NHE1immunoreactivity was expressed in the SP. In the IPC + ischemia-operated-groups, NHE1 immunoreactivity was also expressed in the SP of the CA1-3; however, the immunoreactivity was more slightly changed than that in the ischemia-operated-groups. In brief, our findings show that IPC dramatically protected CA1 pyramidal neurons and strongly inhibited NHE1 expression in the SP of the CA1 after ischemia–reperfusion. These findings suggest that the inhibition of NHE1 expression may be necessary for neuronal survival from transient ischemic damage.
