PMID- 22408607
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20121002
LR  - 20211021
IS  - 1662-5102 (Electronic)
IS  - 1662-5102 (Linking)
VI  - 6
DP  - 2012
TI  - Dynamic regulation of NMDAR function in the adult brain by the stress hormone 
      corticosterone.
PG  - 9
LID - 10.3389/fncel.2012.00009 [doi]
LID - 9
AB  - Stress and corticosteroids dynamically modulate the expression of synaptic 
      plasticity at glutamatergic synapses in the developed brain. Together with 
      alpha-amino-3-hydroxy-methyl-4-isoxazole propionic acid receptors (AMPAR), 
      N-methyl-D-aspartate receptors (NMDAR) are critical mediators of synaptic 
      function and are essential for the induction of many forms of synaptic 
      plasticity. Regulation of NMDAR function by cortisol/corticosterone (CORT) may be 
      fundamental to the effects of stress on synaptic plasticity. Recent reports of 
      the efficacy of NMDAR antagonists in treating certain stress-associated 
      psychopathologies further highlight the importance of understanding the 
      regulation of NMDAR function by CORT. Knowledge of how corticosteroids regulate 
      NMDAR function within the adult brain is relatively sparse, perhaps due to a 
      common belief that NMDAR function is stable in the adult brain. We review recent 
      results from our laboratory and others demonstrating dynamic regulation of NMDAR 
      function by CORT in the adult brain. In addition, we consider the issue of how 
      differences in the early life environment may program differential sensitivity to 
      modulation of NMDAR function by CORT and how this may influence synaptic function 
      during stress. Findings from these studies demonstrate that NMDAR function in the 
      adult hippocampus remains sensitive to even brief exposures to CORT and that the 
      capacity for modulation of NMDAR may be programmed, in part, by the early life 
      environment. Modulation of NMDAR function may contribute to dynamic regulation of 
      synaptic plasticity and adaptation in the face of stress, however, enhanced NMDAR 
      function may be implicated in mechanisms of stress-related psychopathologies 
      including depression.
FAU - Tse, Yiu Chung
AU  - Tse YC
AD  - Neuroscience Division, Douglas Mental Health University Institute, McGill 
      University, Montreal QC, Canada.
FAU - Bagot, Rosemary C
AU  - Bagot RC
FAU - Wong, Tak Pan
AU  - Wong TP
LA  - eng
PT  - Journal Article
DEP - 20120306
PL  - Switzerland
TA  - Front Cell Neurosci
JT  - Frontiers in cellular neuroscience
JID - 101477935
PMC - PMC3294281
OTO - NOTNLM
OT  - corticosteroid receptor
OT  - electrophysiology
OT  - learning and memory
OT  - receptor trafficking
OT  - stress
OT  - synaptic plasticity
EDAT- 2012/03/13 06:00
MHDA- 2012/03/13 06:01
PMCR- 2012/01/01
CRDT- 2012/03/13 06:00
PHST- 2011/11/15 00:00 [received]
PHST- 2012/02/17 00:00 [accepted]
PHST- 2012/03/13 06:00 [entrez]
PHST- 2012/03/13 06:00 [pubmed]
PHST- 2012/03/13 06:01 [medline]
PHST- 2012/01/01 00:00 [pmc-release]
AID - 10.3389/fncel.2012.00009 [doi]
PST - epublish
SO  - Front Cell Neurosci. 2012 Mar 6;6:9. doi: 10.3389/fncel.2012.00009. eCollection 
      2012.