Shimazaki K, Ishida A, Rhee S G, Takenawa T, Kawai N
Department of Physiology, Jichi Medical School, Tochigi-ken, Japan.
Neuroreport. 1994 Mar 21;5(7):785-8. doi: 10.1097/00001756-199403000-00012.
The distribution of inositol 1,4,5-triphosphate 3-kinase (IP3 3-kinase) in the gerbil hippocampus was studied before and after transient ischaemia, by immunohistochemistry and immunoblot with monoclonal antibody to IP3 3-kinase. In control gerbils, intense IP3 3-kinase immunoreactivity was localized in the dendritic field of CA1 pyramidal neurones. However, after ischaemia for 5 min, the immunoreactivity decreased gradually, until after 24 h there was very little IP3 3-kinase detectable. Immunoblot study showed a similar decrease of IP3 3-kinase in ischaemic hippocampus. Infliction of 2 min ischaemia prior to the 5 min of ischaemia is known to have a protective effect on the 5 min ischaemia. With the addition of the 2 min ischaemia there was no decrease in IP3 3-kinase following the 5 min ischaemia. The results suggest that IP3 3-kinase might play a critical role in inducing the delayed neuronal death following ischaemia.