PMID- 19893758
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20110714
LR  - 20211020
IS  - 1662-5099 (Electronic)
IS  - 1662-5099 (Linking)
VI  - 2
DP  - 2009
TI  - Synaptic NR2A- but not NR2B-Containing NMDA Receptors Increase with Blockade of 
      Ionotropic Glutamate Receptors.
PG  - 19
LID - 10.3389/neuro.02.019.2009 [doi]
LID - 19
AB  - NMDA receptors (NMDAR) are key molecules involved in physiological and 
      pathophysiological brain processes such as plasticity and excitotoxicity. 
      Neuronal activity regulates NMDA receptor levels in the cell membrane. However, 
      little is known on which time scale this regulation occurs and whether the two 
      main diheteromeric NMDA receptor subtypes in forebrain, NR1/NR2A and NR1/NR2B, 
      are regulated in a similar fashion. As these differ considerably in their 
      electrophysiological properties, the NR2A/NR2B ratio affects the neurons' 
      reaction to NMDA receptor activation. Here we provide evidence that the basal 
      turnover rate in the cell membrane of NR2A- and NR2B-containing receptors is 
      comparable. However, the level of the NR2A subtype in the cell membrane is highly 
      regulated by NMDA receptor activity, resulting in a several-fold increased 
      insertion of new receptors after blocking NMDAR for 8 h. Blocking AMPA receptors 
      also increases the delivery of NR2A-containing receptors to the cell membrane. In 
      contrast, the amount of NR2B-containing receptors in the cell membrane is not 
      affected by ionotropic glutamate receptor block. Moreover, electrophysiological 
      analysis of synaptic currents in hippocampal cultures and CA1 neurons of 
      hippocampal slices revealed that after 8 h of NMDA receptor blockade the NMDA 
      EPSCs increase as a result of augmented NMDA receptor-mediated currents. In 
      conclusion, synaptic NR2A- but not NR2B-containing receptors are dynamically 
      regulated, enabling neurons to change their NR2A/NR2B ratio within a time scale 
      of hours.
FAU - von Engelhardt, Jakob
AU  - von Engelhardt J
AD  - Department of Clinical Neurobiology, University of Heidelberg Heidelberg, 
      Germany.
FAU - Doganci, Beril
AU  - Doganci B
FAU - Seeburg, Peter H
AU  - Seeburg PH
FAU - Monyer, Hannah
AU  - Monyer H
LA  - eng
PT  - Journal Article
DEP - 20091026
PL  - Switzerland
TA  - Front Mol Neurosci
JT  - Frontiers in molecular neuroscience
JID - 101477914
PMC - PMC2773170
OTO - NOTNLM
OT  - APV
OT  - MK-801
OT  - NVP-AAM077
OT  - ifenprodil
OT  - mouse
EDAT- 2009/11/07 06:00
MHDA- 2009/11/07 06:01
PMCR- 2009/01/01
CRDT- 2009/11/07 06:00
PHST- 2009/01/13 00:00 [received]
PHST- 2009/10/01 00:00 [accepted]
PHST- 2009/11/07 06:00 [entrez]
PHST- 2009/11/07 06:00 [pubmed]
PHST- 2009/11/07 06:01 [medline]
PHST- 2009/01/01 00:00 [pmc-release]
AID - 10.3389/neuro.02.019.2009 [doi]
PST - epublish
SO  - Front Mol Neurosci. 2009 Oct 26;2:19. doi: 10.3389/neuro.02.019.2009. eCollection 
      2009.