PMID- 25520615
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20141218
LR  - 20200930
IS  - 1662-5099 (Print)
IS  - 1662-5099 (Electronic)
IS  - 1662-5099 (Linking)
VI  - 7
DP  - 2014
TI  - Age dependence of the rapid antidepressant and synaptic effects of acute NMDA 
      receptor blockade.
PG  - 94
LID - 10.3389/fnmol.2014.00094 [doi]
LID - 94
AB  - Ketamine is a N-methyl-D-aspartate receptor (NMDAR) antagonist that produces 
      rapid antidepressant responses in individuals with major depressive disorder. The 
      antidepressant action of ketamine has been linked to blocking NMDAR activation at 
      rest, which inhibits eukaryotic elongation factor 2 kinase leading to 
      desuppression of protein synthesis and synaptic potentiation in the CA1 region of 
      the hippocampus. Here, we investigated ketamine mediated antidepressant response 
      and the resulting synaptic potentiation in juvenile animals. We found that 
      ketamine did not produce an antidepressant response in juvenile animals in the 
      novelty suppressed feeding or the forced swim test. In addition ketamine 
      application failed to trigger synaptic potentiation in hippocampal slices 
      obtained from juvenile animals, unlike its action in slices from adult animals. 
      The inability of ketamine to trigger an antidepressant response or subsequent 
      synaptic plasticity processes suggests a developmental component to ketamine 
      mediated antidepressant efficacy. We also show that the NMDAR antagonist AP5 
      triggers synaptic potentiation in mature hippocampus similar to the action of 
      ketamine, demonstrating that global competitive blockade of NMDARs is sufficient 
      to trigger this effect. These findings suggest that global blockade of NMDARs in 
      developmentally mature hippocampal synapses are required for the antidepressant 
      efficacy of ketamine.
FAU - Nosyreva, Elena
AU  - Nosyreva E
AD  - Department of Neuroscience, University of Texas Southwestern Medical Center 
      Dallas, TX, USA.
FAU - Autry, Anita E
AU  - Autry AE
AD  - Department of Neuroscience, University of Texas Southwestern Medical Center 
      Dallas, TX, USA.
FAU - Kavalali, Ege T
AU  - Kavalali ET
AD  - Department of Neuroscience, University of Texas Southwestern Medical Center 
      Dallas, TX, USA.
FAU - Monteggia, Lisa M
AU  - Monteggia LM
AD  - Department of Neuroscience, University of Texas Southwestern Medical Center 
      Dallas, TX, USA.
LA  - eng
GR  - R01 MH066198/MH/NIMH NIH HHS/United States
GR  - R01 MH070727/MH/NIMH NIH HHS/United States
PT  - Journal Article
DEP - 20141201
PL  - Switzerland
TA  - Front Mol Neurosci
JT  - Frontiers in molecular neuroscience
JID - 101477914
PMC - PMC4249453
OTO - NOTNLM
OT  - antidepressant
OT  - behavior
OT  - development
OT  - ketamine
OT  - synaptic potentiation
EDAT- 2014/12/19 06:00
MHDA- 2014/12/19 06:01
PMCR- 2014/01/01
CRDT- 2014/12/19 06:00
PHST- 2014/08/27 00:00 [received]
PHST- 2014/11/11 00:00 [accepted]
PHST- 2014/12/19 06:00 [entrez]
PHST- 2014/12/19 06:00 [pubmed]
PHST- 2014/12/19 06:01 [medline]
PHST- 2014/01/01 00:00 [pmc-release]
AID - 10.3389/fnmol.2014.00094 [doi]
PST - epublish
SO  - Front Mol Neurosci. 2014 Dec 1;7:94. doi: 10.3389/fnmol.2014.00094. eCollection 
      2014.