PMID- 28133447
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 1662-5153 (Print)
IS  - 1662-5153 (Electronic)
IS  - 1662-5153 (Linking)
VI  - 10
DP  - 2016
TI  - GluN1 and GluN2A NMDA Receptor Subunits Increase in the Hippocampus during Memory 
      Consolidation in the Rat.
PG  - 242
LID - 10.3389/fnbeh.2016.00242 [doi]
LID - 242
AB  - It is widely accepted that NMDA receptors (NMDAR) are required for learning and 
      memory formation, and for synaptic plasticity induction. We have previously shown 
      that hippocampal GluN1 and GluN2A NMDAR subunits significantly increased 
      following habituation of rats to an open field (OF), while GluN2B remained 
      unchanged. Similar results were obtained after CA1-long-term potentiation (LTP) 
      induction in rat hippocampal slices. Other studies have also shown NMDAR up 
      regulation at earlier and later time points after LTP induction or learning 
      acquisition. In this work, we have studied NMDAR subunits levels in the 
      hippocampus and prefrontal cortex (PFC) after OF habituation and after object 
      recognition (OR), to find out whether rising of NMDAR subunits is a general and 
      structure-specific feature during memory formation. In 1, 2 and 3 month old rats 
      there was an increase in hippocampal GluN1 and GluN2A, but not in GluN2B levels 
      70 min after OF habituation. This rise overlaps with early phase of memory 
      consolidation, suggesting a putative relationship between them. The increases 
      fell down to control levels 90 min after training. Similar results were obtained 
      in the hippocampus of adult rats 70 min after OR training, without changes in 
      PFC. Following OF test or OR discrimination phase, NMDAR subunits remained 
      unchanged. Hence, rising of hippocampal GluN1 and GluN2A appears to be a general 
      feature after novel "spatial/discrimination" memory acquisition. To start 
      investigating the dynamics and possible mechanisms of these changes, we have 
      studied hippocampal neuron cultures stimulated by KCl to induce plasticity. GluN1 
      and GluN2A increased both in dendrites and neuronal bodies, reaching a maximum 75 
      min later and returning to control levels at 90 min. Translation and/or 
      transcription and mobilization differentially contribute to this rise in subunits 
      in bodies and dendrites. Our results showed that the NMDAR subunits increase 
      follows a similar time course both in vitro and in vivo. These changes happen in 
      the hippocampus where a spatial representation of the environment is being formed 
      making possible short term and long term memories (STM and LTM); appear to be 
      structure-specific; are preserved along life; and could be related to synaptic 
      tagging and/or to memory consolidation of new spatial/discrimination information.
FAU - Cercato, Magali C
AU  - Cercato MC
AD  - Laboratorio de Neuroplasticidad y Neurotoxinas, Instituto de Biologia Celular y 
      Neurociencia, Universidad de Buenos Aires (UBA)-CONICET Buenos Aires, Argentina.
FAU - Vazquez, Cecilia A
AU  - Vazquez CA
AD  - Laboratorio de Neuroplasticidad y Neurotoxinas, Instituto de Biologia Celular y 
      Neurociencia, Universidad de Buenos Aires (UBA)-CONICET Buenos Aires, Argentina.
FAU - Kornisiuk, Edgar
AU  - Kornisiuk E
AD  - Laboratorio de Neuroplasticidad y Neurotoxinas, Instituto de Biologia Celular y 
      Neurociencia, Universidad de Buenos Aires (UBA)-CONICET Buenos Aires, Argentina.
FAU - Aguirre, Alejandra I
AU  - Aguirre AI
AD  - Laboratorio de Neuroplasticidad y Neurotoxinas, Instituto de Biologia Celular y 
      Neurociencia, Universidad de Buenos Aires (UBA)-CONICET Buenos Aires, Argentina.
FAU - Colettis, Natalia
AU  - Colettis N
AD  - Laboratorio de Neuroplasticidad y Neurotoxinas, Instituto de Biologia Celular y 
      Neurociencia, Universidad de Buenos Aires (UBA)-CONICET Buenos Aires, Argentina.
FAU - Snitcofsky, Marina
AU  - Snitcofsky M
AD  - Laboratorio de Neuroplasticidad y Neurotoxinas, Instituto de Biologia Celular y 
      Neurociencia, Universidad de Buenos Aires (UBA)-CONICET Buenos Aires, Argentina.
FAU - Jerusalinsky, Diana A
AU  - Jerusalinsky DA
AD  - Laboratorio de Neuroplasticidad y Neurotoxinas, Instituto de Biologia Celular y 
      Neurociencia, Universidad de Buenos Aires (UBA)-CONICETBuenos Aires, Argentina; 
      Ciclo Basico Comun-Universidad de Buenos AiresBuenos Aires, Argentina.
FAU - Baez, Maria V
AU  - Baez MV
AD  - Laboratorio de Neuroplasticidad y Neurotoxinas, Instituto de Biologia Celular y 
      Neurociencia, Universidad de Buenos Aires (UBA)-CONICETBuenos Aires, Argentina; 
      1UA de Biologia Celular, Histologia, Embriologia y Genetica, Departamento de 
      Histologia, Facultad de Medicina, Universidad de Buenos AiresBuenos Aires, 
      Argentina.
LA  - eng
PT  - Journal Article
DEP - 20170113
PL  - Switzerland
TA  - Front Behav Neurosci
JT  - Frontiers in behavioral neuroscience
JID - 101477952
PMC - PMC5233710
OTO - NOTNLM
OT  - GluN1
OT  - GluN2A
OT  - LTM
OT  - NMDAR
OT  - hippocampus
OT  - synaptic plasticity
EDAT- 2017/01/31 06:00
MHDA- 2017/01/31 06:01
PMCR- 2016/01/01
CRDT- 2017/01/31 06:00
PHST- 2016/08/17 00:00 [received]
PHST- 2016/12/12 00:00 [accepted]
PHST- 2017/01/31 06:00 [entrez]
PHST- 2017/01/31 06:00 [pubmed]
PHST- 2017/01/31 06:01 [medline]
PHST- 2016/01/01 00:00 [pmc-release]
AID - 10.3389/fnbeh.2016.00242 [doi]
PST - epublish
SO  - Front Behav Neurosci. 2017 Jan 13;10:242. doi: 10.3389/fnbeh.2016.00242. 
      eCollection 2016.