PMID- 12040047
OWN - NLM
STAT- MEDLINE
DCOM- 20020705
LR  - 20231014
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Print)
IS  - 0270-6474 (Linking)
VI  - 22
IP  - 11
DP  - 2002 Jun 1
TI  - Multiple mechanisms for the potentiation of AMPA receptor-mediated transmission 
      by alpha-Ca2+/calmodulin-dependent protein kinase II.
PG  - 4406-11
AB  - Some forms of activity-dependent synaptic potentiation require the activation of 
      postsynaptic Ca(2+)/calmodulin-dependent protein kinase II (CaMKII). Activation 
      of CaMKII has been shown to phosphorylate the glutamate receptor 1 subunit of the 
      AMPA receptor (AMPAR), thereby affecting some of the properties of the receptor. 
      Here, a recombinant, constitutively active form of alphaCaMKII tagged with the 
      fluorescent marker green fluorescent protein (GFP) [alphaCaMKII(1-290)-enhanced 
      GFP (EGFP)] was expressed in CA1 pyramidal neurons from hippocampal slices. The 
      changes in glutamatergic transmission onto these cells were analyzed. AMPA but 
      not NMDA receptor-mediated EPSCs were specifically potentiated in infected 
      compared with nearby noninfected neurons. This potentiation was associated with a 
      reduction in the proportion of synapses devoid of AMPARs. In addition, expression 
      of alphaCaMKII(1-290)-EGFP increased the quantal size of AMPAR-mediated 
      responses. This effect reflected, at least in part, an increased unitary 
      conductance of the channels underlying the EPSCs. These results reveal that 
      several key features of long-term potentiation of hippocampal glutamatergic 
      synapses are reproduced by the sole activity of alphaCaMKII.
FAU - Poncer, Jean Christophe
AU  - Poncer JC
AD  - Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA. 
      jcponcer@biomedicale.univ-paris5.fr
FAU - Esteban, Jose A
AU  - Esteban JA
FAU - Malinow, Roberto
AU  - Malinow R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (Luminescent Proteins)
RN  - 0 (Receptors, AMPA)
RN  - 0 (Recombinant Fusion Proteins)
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/genetics/*metabolism
MH  - Excitatory Postsynaptic Potentials/physiology
MH  - Female
MH  - Gene Expression
MH  - Hippocampus/cytology/metabolism
MH  - In Vitro Techniques
MH  - Long-Term Potentiation/*physiology
MH  - Luminescent Proteins/genetics
MH  - Male
MH  - Neuronal Plasticity/physiology
MH  - Patch-Clamp Techniques
MH  - Pyramidal Cells/metabolism
MH  - Rats
MH  - Receptors, AMPA/*metabolism
MH  - Recombinant Fusion Proteins/genetics/metabolism
MH  - Sindbis Virus/genetics
MH  - Synaptic Transmission/*physiology
MH  - Transgenes
PMC - PMC6758819
EDAT- 2002/06/01 10:00
MHDA- 2002/07/06 10:01
PMCR- 2002/12/01
CRDT- 2002/06/01 10:00
PHST- 2002/06/01 10:00 [pubmed]
PHST- 2002/07/06 10:01 [medline]
PHST- 2002/06/01 10:00 [entrez]
PHST- 2002/12/01 00:00 [pmc-release]
AID - 22/11/4406 [pii]
AID - 6449 [pii]
AID - 10.1523/JNEUROSCI.22-11-04406.2002 [doi]
PST - ppublish
SO  - J Neurosci. 2002 Jun 1;22(11):4406-11. doi: 10.1523/JNEUROSCI.22-11-04406.2002.