Changes in IP3 3-kinase immunoreactivity following transient ischaemia in gerbil hippocampus.
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.
Shimazaki
K
K
Department of Physiology, Jichi Medical School, Tochigi-ken, Japan.
Ishida
A
A
Rhee
S G
SG
Takenawa
T
T
Kawai
N
N
D000818:Animals; D002118:Calcium / Q000378:metabolism; D005849:Gerbillinae; D006624:Hippocampus / Q000378:metabolism* / Q000473:pathology; D015151:Immunoblotting; D007150:Immunohistochemistry; D002546:Ischemic Attack, Transient / Q000378:metabolism* / Q000473:pathology; D009410:Nerve Degeneration; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D017853:Phosphotransferases (Alcohol Group Acceptor) / Q000378:metabolism*
D017853:Phosphotransferases (Alcohol Group Acceptor); C051038:Inositol 1,4,5-trisphosphate 3-kinase; D002118:Calcium