Session: 7

PS7-11 | Pharmacological GluN2A antagonism blocked CAMKII activation thought not GluN1 increased levels after chemical LTP induction

Natalí Shirly Rozic


Synaptic plasticity (SP) involves changes in dendritic spine cytoskeleton, volume, and postsynaptic molecular composition. One of the most studied forms of SP is Long Term potentiation (LTP) that induces dendritic spine maturation and change in NMDA Receptor (NMDAR) composition. It was described that GluN1, and GluN2A NMDAR subunits increase 70 minutes after LTP induction or memory acquisition. GluN2A is considered a marker of mature synapses, however, little is known about its role in LTP induction in part because GluN2A antagonists, as NVP 0077, are recently developed. In our laboratory, we induced chemical LTP in hippocampal cultured neurons and then blocked the GluN2A subunit by NVP-0077. Later, we analyzed molecular dendritic composition by immunofluorescence assays. Preliminary, we found that NVP-0077 blockade inhibits GluN2A but not GluN1 increased dendritic levels 70 minutes after LTP induction. Also, at this time point we observed that CAMKII is not activated, and NF-kB levels are similar to basal levels. Further investigation is needed to establish that GLuN2A increased levels post LTP induction would be a marker for this process.