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Volume 16, Number 19,
Issue of October 1, 1996
pp. 6236-6245
Copyright ©1996 Society for Neuroscience
Specific Induction of Protein Kinase C Subspecies after
Transient Middle Cerebral Artery Occlusion in the Rat
Brain: Inhibition by MK-801
Received Feb. 21, 1996; revised June 10, 1996; accepted July 8, 1996.
Susanna Miettinen1,
Reina Roivainen1,
Riitta Keinänen1,
Tomas Hökfelt2, and
Jari Koistinaho1, 2
1 A. I. Virtanen Institute, University of Kuopio,
FIN-70211 Kuopio, Finland, and 2 Department of
Neuroscience, Karolinska Institute, Stockholm, Sweden
Protein kinase C (PKC) consists of a family of closely related
Ca2+/phospholipid-dependent phosphotransferase isozymes,
most of which are present in the brain and are differentially activated
by second messengers. Calcium-dependent PKC activity may cause neuronal
degeneration after ischemic insult. PKC is also involved in
trophic-factor signaling, indicating that activity of some PKC
subspecies may be beneficial to the injured brain. Therefore, we
screened long-term changes in the expression of multiple PKC subspecies
after focal brain ischemia. Middle cerebral artery occlusion was
produced by using an intraluminal suture for 30 min or 90 min. In
in situ hybridization experiments, mRNA levels of
PKC , - , - , - , - and - were decreased in the infarct
core 4 hr after ischemia and were lost completely 12 hr after ischemia.
In areas surrounding the core, PKC mRNA was specifically induced 4, 12, and 24 hr after ischemia in the cortex. At 3 and 7 d, the core
and a rim around it showed increased mRNA levels of PKC. No other
subspecies were induced. At 2 d, immunoblotting demonstrated
increased levels of PKC protein in the perifocal tissue, and
immunocytochemistry revealed an increased number of PKC-positive
neurons in the perifocal cortex. In the core, PKC-positive
macrophages and endothelial cells were seen. Pretreatment with MK-801,
an NMDA antagonist, inhibited cortical PKC mRNA induction. The data
show that focal brain ischemia induces PKC mRNA and protein but not
other PKC subspecies through the activation of NMDA receptors and that
the upregulation lasts for several days in neurons of the perifocal
zone.
Key words:
phosphorylation;
protein kinase C;
brain ischemia;
gene expression;
penumbra;
cortex;
striatum;
glutamate
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