Journal
CURRENT OPINION IN NEUROBIOLOGY
Volume 51, Issue -, Pages 1-7Publisher
CURRENT BIOLOGY LTD
DOI: 10.1016/j.conb.2017.12.020
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Funding
- NIH [EY025668]
- Allen Institute for Brain Science
- MINECO [BFU2015-68655-P]
- Royal Society International Exchanges Grant
- BBSRC
- CIHR [OG 126137, NIA 288936]
- NSERC [DG 2017-04730, DAS 2017-507818]
- BBSRC [BB/H002383/2] Funding Source: UKRI
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In the classical view, postsynaptic NMDA receptors (NMDARs) trigger Hebbian plasticity via Ca2+ influx. However, unconventional presynaptic NMDARs (preNMDARs) which regulate both long-term and short-term plasticity at several synapse types have also been found. A lack of sufficiently specific experimental manipulations and a poor understanding of how preNMDARs signal have contributed to long-standing controversy surrounding these receptors. Although several prior studies linked preNMDARs to neocortical timing dependent long-term depression (tLTD), a recent study argues that the NMDARs are actually postsynaptic and signal metabotropically, that is, without Ca2+. Other recent work indicates that, whereas ionotropic preNMDARs signaling controls evoked release, spontaneous release is regulated by metabotropic NMDAR signaling. We argue that elucidating unconventional NMDAR signaling modes - both presynaptically and metabotropically - is key to resolving the preNMDAR debate.
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