Presence of calcium/calmodulin-dependent protein Kinase II in Nerve terminals of rat brain

Synapse ◽  
1989 ◽  
Vol 3 (4) ◽  
pp. 356-362 ◽  
Author(s):  
S. Ivar Walaas ◽  
Fred S. Gorelick ◽  
Paul Greengard
Keyword(s):  
Protein Kinase ◽  
Rat Brain ◽  
Nerve Terminals ◽  
Dependent Protein Kinase ◽  
Calcium Calmodulin Dependent ◽  
Protein Kinase Ii ◽  
Dependent Protein

Regional alterations of JNK3 and CaMKIIα subunit expression in the rat brain after soman poisoning

2010 ◽  
Vol 30 (6) ◽  
pp. 448-459 ◽  
Author(s):  
G. RamaRao ◽  
CK Waghmare ◽  
Nalini Srivastava ◽  
BK Bhattacharya
Keyword(s):  
Cerebral Cortex ◽  
Protein Kinase ◽  
Rat Brain ◽  
Protein Kinases ◽  
Nerve Agent ◽  
Dependent Protein Kinase ◽  
Altered Expression ◽  
Calcium Calmodulin Dependent ◽  
Protein Kinase Ii ◽  
Dependent Protein

Calcium/calmodulin-dependent protein kinase II (CaMKII) and c-Jun N-terminal kinases (JNKs) exert numerous and diverse functions in the brain. However, their role in nerve agent poisoning is poorly understood. In the present study, rats were exposed to soman (80 µg/kg) subcutaneously to study the changes in the protein levels of calcium/calmodulin-dependent protein kinase II alpha subunit (CaMKIIα) and JNK3 and activities of acetylcholinestarase (AChE) and CaMKII in the rat brain. Western blot analysis revealed that significant changes were found in both the protein kinases expression. Immunoreactivity levels of neural specific JNK3 isoform increased from 2.5 hours to 30 days after soman exposure in cerebral cortex, hippocampus, striatum and thalamus regions and decreased in the case of cerebellum. CaMKIIα expression levels were also increased from 2.5 hours to 30 days after soman exposure in cerebral cortex, hippocampus, thalamus and down regulated in cerebellum. AChE activity remained inhibited in plasma and brain up to 3 days post exposure. CaMKII activity was increased in cerebrum and decreased in cerebellum. Results suggest that altered expression of both the protein kinases play a role in nerve agent-induced long-term neurotoxic effects.

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