PMID- 19118199
OWN - NLM
STAT- MEDLINE
DCOM- 20090213
LR  - 20211020
IS  - 1091-6490 (Electronic)
IS  - 0027-8424 (Print)
IS  - 0027-8424 (Linking)
VI  - 106
IP  - 2
DP  - 2009 Jan 13
TI  - G protein-activated inwardly rectifying potassium channels mediate depotentiation 
      of long-term potentiation.
PG  - 635-40
LID - 10.1073/pnas.0811685106 [doi]
AB  - Excitatory synapses in the brain undergo activity-dependent changes in the 
      strength of synaptic transmission. Such synaptic plasticity as exemplified by 
      long-term potentiation (LTP) is considered a cellular correlate of learning and 
      memory. The presence of G protein-activated inwardly rectifying K(+) (GIRK) 
      channels near excitatory synapses on dendritic spines suggests their possible 
      involvement in synaptic plasticity. However, whether activity-dependent 
      regulation of GIRK channels affects excitatory synaptic plasticity is unknown. In 
      a companion article we have reported activity-dependent regulation of GIRK 
      channel density in cultured hippocampal neurons that requires activity of NMDA 
      receptors (NMDAR) and protein phosphatase-1 (PP1) and takes place within 15 min. 
      In this study, we performed whole-cell recordings of cultured hippocampal neurons 
      and found that NMDAR activation increases basal GIRK current and GIRK channel 
      activation mediated by adenosine A(1) receptors, but not GABA(B) receptors. Given 
      the similar involvement of NMDARs, adenosine A(1) receptors, and PP1 in 
      depotentiation of LTP caused by low-frequency stimulation that immediately 
      follows LTP-inducing high-frequency stimulation, we wondered whether 
      NMDAR-induced increase in GIRK channel surface density and current may contribute 
      to the molecular mechanisms underlying this specific depotentiation. Remarkably, 
      GIRK2 null mutation or GIRK channel blockade abolishes depotentiation of LTP, 
      demonstrating that GIRK channels are critical for depotentiation, one form of 
      excitatory synaptic plasticity.
FAU - Chung, Hee Jung
AU  - Chung HJ
AD  - Howard Hughes Medical Institute and Department of Physiology, University of 
      California, San Francisco, CA 94158, USA.
FAU - Ge, Woo-Ping
AU  - Ge WP
FAU - Qian, Xiang
AU  - Qian X
FAU - Wiser, Ofer
AU  - Wiser O
FAU - Jan, Yuh Nung
AU  - Jan YN
FAU - Jan, Lily Yeh
AU  - Jan LY
LA  - eng
GR  - R01 MH065334/MH/NIMH NIH HHS/United States
GR  - R37 MH065334/MH/NIMH NIH HHS/United States
GR  - HHMI/Howard Hughes Medical Institute/United States
GR  - MH65334/MH/NIMH NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20081231
PL  - United States
TA  - Proc Natl Acad Sci U S A
JT  - Proceedings of the National Academy of Sciences of the United States of America
JID - 7505876
RN  - 0 (G Protein-Coupled Inwardly-Rectifying Potassium Channels)
RN  - 0 (Kcnj6 protein, rat)
RN  - 0 (Receptor, Adenosine A1)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
SB  - IM
MH  - Animals
MH  - Dendritic Spines
MH  - Electrophysiology
MH  - G Protein-Coupled Inwardly-Rectifying Potassium Channels/*physiology
MH  - Hippocampus/cytology
MH  - Long-Term Potentiation/*physiology
MH  - *Long-Term Synaptic Depression
MH  - Neuronal Plasticity
MH  - Neurons/chemistry/physiology
MH  - Rats
MH  - Receptor, Adenosine A1/physiology
MH  - Receptors, N-Methyl-D-Aspartate/metabolism
MH  - Synapses
PMC - PMC2613041
COIS- The authors declare no conflict of interest.
EDAT- 2009/01/02 09:00
MHDA- 2009/02/14 09:00
PMCR- 2008/12/31
CRDT- 2009/01/02 09:00
PHST- 2009/01/02 09:00 [entrez]
PHST- 2009/01/02 09:00 [pubmed]
PHST- 2009/02/14 09:00 [medline]
PHST- 2008/12/31 00:00 [pmc-release]
AID - 0811685106 [pii]
AID - 6219 [pii]
AID - 10.1073/pnas.0811685106 [doi]
PST - ppublish
SO  - Proc Natl Acad Sci U S A. 2009 Jan 13;106(2):635-40. doi: 
      10.1073/pnas.0811685106. Epub 2008 Dec 31.