PMID- 16515554
OWN - NLM
STAT- MEDLINE
DCOM- 20060518
LR  - 20191210
IS  - 0022-3042 (Print)
IS  - 0022-3042 (Linking)
VI  - 97
IP  - 1
DP  - 2006 Apr
TI  - Decreased calcium/calmodulin-dependent protein kinase II and protein kinase C 
      activities mediate impairment of hippocampal long-term potentiation in the 
      olfactory bulbectomized mice.
PG  - 22-9
AB  - Olfactory bulbectomized (OBX) mice showed significant impairment of learning and 
      memory-related behaviors 14 days after olfactory bulbectomy, as measured by 
      passive avoidance and Y-maze tasks. We here observed a large impairment of 
      hippocampal long-term potentiation (LTP) in the OBX mice. Concomitant with 
      decreased acetylcholinesterase expression, protein kinase C (PKC)alpha 
      autophosphorylation and NR1(Ser-896) phosphorylation significantly decreased in 
      the hippocampal CA1 region of OBX mice. Both PKCalpha and NR1(Ser-896) 
      phosphorylation significantly increased following LTP in the control mice, 
      whereas increases were not observed in OBX mice. Like PKC activities, 
      calcium/calmodulin-dependent protein kinase II (CaMKII) autophosphorylation 
      significantly decreased in the hippocampal CA1 region of OBX mice as compared 
      with that of control mice. In addition, increased CaMKII autophosphorylation 
      following LTP was not observed in OBX mice. Finally, the impairment of CaMKII 
      autophosphorylation was closely associated with reduced pGluR1(Ser-831) 
      phosphorylation, without change in synapsin I (site 3) phosphorylation in the 
      hippocampal CA1 region of OBX mice. Taken together, in OBX mice NMDA receptor 
      hypofunction, possibly through decreased PKCalpha activity, underlies decreased 
      CaMKII activity in the post-synaptic regions, thereby impairing LTP induction in 
      the hippocampal CA1 region. Both decreased PKC and CaMKII activities with 
      concomitant LTP impairment account for the learning disability observed in OBX 
      mice.
FAU - Moriguchi, Shigeki
AU  - Moriguchi S
AD  - Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Tohoku 
      University, Sendai, Japan. shigeki@mail.pharm.tohoku.ac.jp
FAU - Han, Feng
AU  - Han F
FAU - Nakagawasai, Osamu
AU  - Nakagawasai O
FAU - Tadano, Takeshi
AU  - Tadano T
FAU - Fukunaga, Kohji
AU  - Fukunaga K
LA  - eng
PT  - Journal Article
DEP - 20060303
PL  - England
TA  - J Neurochem
JT  - Journal of neurochemistry
JID - 2985190R
RN  - 0 (NR1 NMDA receptor)
RN  - 0 (Receptors, AMPA)
RN  - 0 (Receptors, Metabotropic Glutamate)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 0 (metabotropic glutamate receptor type 1)
RN  - EC 2.7.11.13 (Protein Kinase C-alpha)
RN  - EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinase Type 2)
RN  - EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinases)
RN  - EC 3.1.1.7 (Acetylcholinesterase)
RN  - N9YNS0M02X (Acetylcholine)
SB  - IM
MH  - Acetylcholine/metabolism
MH  - Acetylcholinesterase/metabolism
MH  - Alzheimer Disease/metabolism/physiopathology
MH  - Animals
MH  - Calcium-Calmodulin-Dependent Protein Kinase Type 2
MH  - Calcium-Calmodulin-Dependent Protein Kinases/*metabolism
MH  - Cholinergic Fibers/metabolism/pathology
MH  - Denervation/*adverse effects
MH  - Disease Models, Animal
MH  - Down-Regulation/physiology
MH  - Efferent Pathways/injuries/metabolism/physiopathology
MH  - Hippocampus/*metabolism/physiopathology
MH  - Learning Disabilities/metabolism/physiopathology
MH  - Long-Term Potentiation/*physiology
MH  - Male
MH  - Memory Disorders/metabolism/physiopathology
MH  - Mice
MH  - Olfactory Bulb/*injuries/metabolism/physiopathology
MH  - Organ Culture Techniques
MH  - Phosphorylation
MH  - Protein Kinase C-alpha/*metabolism
MH  - Receptors, AMPA/metabolism
MH  - Receptors, Metabotropic Glutamate/metabolism
MH  - Receptors, N-Methyl-D-Aspartate/*metabolism
MH  - Signal Transduction/physiology
EDAT- 2006/03/07 09:00
MHDA- 2006/05/19 09:00
CRDT- 2006/03/07 09:00
PHST- 2006/03/07 09:00 [pubmed]
PHST- 2006/05/19 09:00 [medline]
PHST- 2006/03/07 09:00 [entrez]
AID - JNC3710 [pii]
AID - 10.1111/j.1471-4159.2006.03710.x [doi]
PST - ppublish
SO  - J Neurochem. 2006 Apr;97(1):22-9. doi: 10.1111/j.1471-4159.2006.03710.x. Epub 
      2006 Mar 3.