Glucokinase plays a key role in the control of blood glucose homeostasis. We investigated the effect of ischemic preconditioning on immunoreactivities of GK and its regulatory protein following 5 min of transient cerebral ischemia in gerbils. The gerbils were randomly assigned to 4 groups. IPC was induced by subjecting the gerbils to 2 min of ischemia followed by 1 day of recovery. In the ischemia-operated-group, a significant loss of neurons was observed in the stratum pyramidale (SP) of the hippocampal CA1 region (CA1) at 5 days post-ischemia; however, in the IPC+ischemiaoperated-group, neurons in the SP were well protected. In the immunohistochemical study, immunoreactivities of GK and GKRP in neurons of the SP were distinctively decreased in the CA1, not CA2/3, from 2 days post-ischemia, and hardly detected in the SP at 5 days post-ischemia. In the IPC+ischemia-operated-group, immunoreactivities of GK and GKRP in the SP of the CA1 were similar to those in the sham-group. Our findings show that IPC dramatically maintains immunoreactivities of GK and GKRP in neurons of the SP of the CA1 after ischemia-reperfusion and indicate that GK and GKRP may be necessary for neurons to survive against transient cerebral ischemia.