NMDA receptor-dependent long-term potentiation and long-term depression (LTP/LTD).

By C. Lüscher, R. Malenka. Cold Spring Harbor Perspectives in Biology, 2012

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Mechanisms of neuronal cell death in ischemic stroke and their therapeutic implications (2021, background): “Once glutamate binds to NMDARs, Ca channels are opened.(32)”
Amyloid β-based therapy for Alzheimer’s disease: challenges, successes and future (2023, background): “As a glutamate receptor, functional NMDARs regulate the formation of synapes and synaptic plasticity.(78) AβOs directly disturb the activity of NMDARs and impair NMDAR-mediated signaling pathways (e.”
Role of glutamate and NMDA receptors in Alzheimer’s disease (2016, neutral): “On the contrary, a modest activation of NMDARs causes a modest increase in postsynaptic Ca 2 + and triggers phosphatase-mediated long-term depression [15].”
Synaptic Plasticity Forms and Functions. (2020, background): “The overlap of these two signals initiates synaptic plasticity expression mechanisms that are perhaps the same as those found for standard LTP (Luscher & Malenka 2012, Kandel et al. 2014).”
AMPARs and synaptic plasticity: the last 25 years. (2013, neutral): “, 2012) and AMPAR trafficking (Anggono and Huganir, 2012; Kessels and Malinow, 2009; Lüscher and Malenka, 2012; Nicoll and Roche, 2013).”
Arc Regulates Experience-Dependent Persistent Firing Patterns in Frontal Cortex (2014, background): “Network mechanisms contribute to persistent activity by recurrent synaptic feedback through AMPARs or NMDARs, which provide greater input selectivity and coding capacity but are less stable.”