PMID- 23490331
OWN - NLM
STAT- MEDLINE
DCOM- 20131113
LR  - 20211021
IS  - 1755-5949 (Electronic)
IS  - 1755-5930 (Print)
IS  - 1755-5930 (Linking)
VI  - 19
IP  - 5
DP  - 2013 May
TI  - The disturbance of hippocampal CaMKII/PKA/PKC phosphorylation in early 
      experimental diabetes mellitus.
PG  - 329-36
LID - 10.1111/cns.12084 [doi]
AB  - BACKGROUND: Defining the impact of diabetes and related risk factors on brain 
      cognitive function is critically important for patients with diabetes. AIMS: To 
      investigate the alterations in hippocampal serine/threonine kinases signaling in 
      the early phase of type 1 and type 2 diabetic rats. METHODS: Early experimental 
      diabetes mellitus was induced in rats with streptozotocin or streptozotocin/high 
      fat. Changes in the phosphorylation of proteins were determined by immunoblotting 
      and immunohistochemistry. RESULTS: Our data showed a pronounced decrease in the 
      phosphorylation of Ca(2+) /calmodulin-dependent protein kinase II (CaMKII) in the 
      hippocampi of both type 1 and type 2 diabetic rats compared with age-matched 
      control rats. Unexpectedly, we found a significant increase in the 
      phosphorylation of synapsin I (Ser 603) and GluR1 (Ser 831) in the same 
      experiment. In addition, aberrant changes in hippocampal protein kinase C (PKC) 
      and protein kinase A (PKA) signaling in type 1 and type 2 diabetic rats were also 
      found. Moreover, PP1alpha and PP2A protein levels were decreased in the hippocampus 
      of type 1 diabetic rats, but significantly up-regulated in type 2 diabetic rats. 
      CONCLUSIONS: The disturbance of CaMKII/PKA/PKC phosphorylation in the hippocampus 
      is an early change that may be associated with the development and progression of 
      diabetes-related cognitive dysfunction.
CI  - (c) 2013 Blackwell Publishing Ltd.
FAU - Liao, Mei-Hua
AU  - Liao MH
AD  - Institute of Pharmacology, Toxicology and Biochemical Pharmaceutics, Zhejiang 
      University, Hangzhou, China.
FAU - Xiang, Ying-Chun
AU  - Xiang YC
FAU - Huang, Ji-Yun
AU  - Huang JY
FAU - Tao, Rong-Rong
AU  - Tao RR
FAU - Tian, Yun
AU  - Tian Y
FAU - Ye, Wei-Feng
AU  - Ye WF
FAU - Zhang, Gen-Sheng
AU  - Zhang GS
FAU - Lu, Ying-Mei
AU  - Lu YM
FAU - Ahmed, Muhammad M
AU  - Ahmed MM
FAU - Liu, Zhi-Rong
AU  - Liu ZR
FAU - Fukunaga, Kohji
AU  - Fukunaga K
FAU - Han, Feng
AU  - Han F
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130314
PL  - England
TA  - CNS Neurosci Ther
JT  - CNS neuroscience & therapeutics
JID - 101473265
RN  - 0 (Receptors, AMPA)
RN  - 0 (Synapsins)
RN  - 5W494URQ81 (Streptozocin)
RN  - EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases)
RN  - EC 2.7.11.13 (Protein Kinase C)
RN  - EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinase Type 2)
RN  - EC 3.1.3.16 (Protein Phosphatase 1)
RN  - EC 3.1.3.16 (Protein Phosphatase 2)
RN  - TFZ3H25BS1 (glutamate receptor ionotropic, AMPA 1)
SB  - IM
MH  - Animals
MH  - Calcium-Calmodulin-Dependent Protein Kinase Type 2/*metabolism
MH  - Cyclic AMP-Dependent Protein Kinases/*metabolism
MH  - Diabetes Mellitus, Experimental/*metabolism
MH  - Hippocampus/*metabolism
MH  - Male
MH  - Phosphorylation
MH  - Protein Kinase C/*metabolism
MH  - Protein Phosphatase 1/analysis
MH  - Protein Phosphatase 2/analysis
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, AMPA/metabolism
MH  - Streptozocin
MH  - Synapsins/metabolism
PMC - PMC6493428
COIS- The authors declare no conflict of interest.
EDAT- 2013/03/16 06:00
MHDA- 2013/11/14 06:00
PMCR- 2013/03/14
CRDT- 2013/03/16 06:00
PHST- 2012/10/10 00:00 [received]
PHST- 2013/02/01 00:00 [revised]
PHST- 2013/02/02 00:00 [accepted]
PHST- 2013/03/16 06:00 [entrez]
PHST- 2013/03/16 06:00 [pubmed]
PHST- 2013/11/14 06:00 [medline]
PHST- 2013/03/14 00:00 [pmc-release]
AID - CNS12084 [pii]
AID - 10.1111/cns.12084 [doi]
PST - ppublish
SO  - CNS Neurosci Ther. 2013 May;19(5):329-36. doi: 10.1111/cns.12084. Epub 2013 Mar 
      14.