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GluN2A and GluN2B subunit-containing NMDA receptors in hippocampal plasticity

Shipton, Olivia A., Paulsen, Ole·2014·Philosophical Transactions of the Royal Society B: Biological Sciences

Abstract

N -Methyl- d -aspartate receptor (NMDAR)-dependent synaptic plasticity is a strong candidate to mediate learning and memory processes that require the hippocampus. This plasticity is bidirectional, and how the same receptor can mediate opposite changes in synaptic weights remains a conundrum. It has been suggested that the NMDAR subunit composition could be involved. Specifically, one subunit composition of NMDARs would be responsible for the induction of long-term potentiation (LTP), whereas NMDARs with a different subunit composition would be engaged in the induction of long-term depression (LTD). Unfortunately, the results from studies that have investigated this hypothesis are contradictory, particularly in relation to LTD. Nevertheless, current evidence does suggest that the GluN2B subunit might be particularly important for plasticity and may make a synapse bidirectionally malleable. In particular, we conclude that the presence of GluN2B subunit-containing NMDARs at the postsynaptic density might be a necessary, though not a sufficient, condition for the strengthening of individual synapses. This is owing to the interaction of GluN2B with calcium/calmodulin-dependent protein kinase II (CaMKII) and is distinct from its contribution as an ion channel.

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  • gluN2B is a receptor essential to form LTP.

    “Among them, miR-223, which targets the AMPA-selective glutamate receptor 2 (GluR2) and the NMDA glutamate receptor gluN2B [33] and miR-181a which regulates only gluN2B [66], a receptor essential to form LTP [8, 71].”

    From Glia-to-neuron transfer of miRNAs via extracellular vesicles: a new mechanism underlying inflammation-induced synaptic alterations (2018) · cites this paper as [71]

    The Summary says GluN2B appears to be a necessary factor for LTP induction under naturalistic conditions. But the Long-term potentiation section says GluN2A-containing receptors alone can trigger a form of LTP, and that blocking GluN2B does not impair LTP under certain protocols. Calling GluN2B unconditionally essential overstates the paper. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

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Cited by

Sorted by citations

Authors
Shipton, O. A., & Paulsen, O.
Venue
Philosophical Transactions of the Royal Society B: Biological Sciences
Published
2014-01-05
Volume
369
Issue
1633
Pages
20130163
ISSN
  • 0962-8436
  • 1471-2970
Cited by
275
References
9
Language
en

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