PMID- 15485503
OWN - NLM
STAT- MEDLINE
DCOM- 20050324
LR  - 20071115
IS  - 0022-3042 (Print)
IS  - 0022-3042 (Linking)
VI  - 91
IP  - 3
DP  - 2004 Nov
TI  - Ca2+/calmodulin-dependent protein kinase II is reversibly autophosphorylated, 
      inactivated and made sedimentable by acute neuronal excitation in rats in vivo.
PG  - 745-54
AB  - Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) is highly enriched in the 
      central nervous system, and is proposed to play important roles in 
      activity-dependent modifications of neuronal functions. We reported previously on 
      the dynamic regulation of the autonomous CaMKII in homogenates from hippocampus 
      and parietal cortex by acute neuronal excitation induced by electroconvulsive 
      treatment (ECT) in rats in vivo. In the present study, we examined in more detail 
      the biochemical changes in CaMKII under such conditions. We unexpectedly found a 
      concurrent increase in autophosphorylation at Thr286(alpha)/287(beta) and 
      decrease in the specific activity of CaMKII in the particulate fraction in either 
      hippocampus or parietal cortex during ECT-induced acute, brief seizure activity. 
      On the other hand, the soluble CaMKII showed a marked decrease in 
      autophosphorylation with unchanged or rather increased specific activity. 
      Increased autophosphorylation and decreased CaMKII activity were associated with 
      the detergent-insoluble particulate fraction. All these changes disappeared soon 
      after the termination of seizure activity. The reversible formation of such an 
      autophosphorylated, inactivated and sedimentable form of CaMKII during acute 
      neuronal excitation may indicate the existence of a novel regulatory mechanism of 
      CaMKII that may be important for normal functioning of the brain.
FAU - Yamagata, Yoko
AU  - Yamagata Y
AD  - Laboratory of Neurochemistry, National Institute for Physiological Sciences, 
      Myodaiji, Okazaki 444-8787, Japan. yamagata@nisp.ac.jp
FAU - Obata, Kunihiko
AU  - Obata K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Neurochem
JT  - Journal of neurochemistry
JID - 2985190R
RN  - 0 (Synapsins)
RN  - EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinase Type 2)
RN  - EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinases)
SB  - IM
MH  - Animals
MH  - Calcium-Calmodulin-Dependent Protein Kinase Type 2
MH  - Calcium-Calmodulin-Dependent Protein Kinases/chemistry/*metabolism
MH  - Disease Progression
MH  - Electroshock
MH  - Enzyme Stability/physiology
MH  - Hippocampus/*enzymology
MH  - Male
MH  - Neurons/*enzymology/*physiology
MH  - Parietal Lobe/*enzymology
MH  - Phosphorylation
MH  - Rats
MH  - Rats, Wistar
MH  - Recovery of Function
MH  - Seizures/*enzymology
MH  - Solubility
MH  - Subcellular Fractions/enzymology
MH  - Synapsins/metabolism
EDAT- 2004/10/16 09:00
MHDA- 2005/03/25 09:00
CRDT- 2004/10/16 09:00
PHST- 2004/10/16 09:00 [pubmed]
PHST- 2005/03/25 09:00 [medline]
PHST- 2004/10/16 09:00 [entrez]
AID - JNC2753 [pii]
AID - 10.1111/j.1471-4159.2004.02753.x [doi]
PST - ppublish
SO  - J Neurochem. 2004 Nov;91(3):745-54. doi: 10.1111/j.1471-4159.2004.02753.x.