Long-term potentiation is independent of the C-tail of the GluA1 AMPA receptor subunit

Díaz-Alonso, Javier; Morishita, Wade; Incontro, Salvatore; Simms, Jeffrey A.; Holtzman, Julia; Gill, Michael; Mucke, Lennart; Malenka, Robert C.; Nicoll, Roger A.

doi:10.7554/elife.58042

Cited by 32 publications

(21 citation statements)

References 35 publications

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“…Most recently, a knock-in mouse study in which the C-terminal domain of endogenous GluA1 was truncated reported no deficit in basal synaptic transmission, LTP, or spatial memory ( Diaz-Alonso et al., 2020 ). These authors propose an alternative model in which it is the number of slots rather than the C-terminal domains of the AMPAR subunits themselves that regulate the extent of AMPAR surface expression and plasticity at synapses ( Diaz-Alonso et al., 2020 ). Thus, it is possible that phosphorylation is required to overcome a yet unidentified, negative modulatory effect, which is lacking in phosphodeficient AMPAR subunits.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, it is possible that phosphorylation is required to overcome a yet unidentified, negative modulatory effect, which is lacking in phosphodeficient AMPAR subunits. Overall, the currently available evidence suggests that plasticity involves the formation/unmasking or removal/masking of slots in the PSD to snare or release passively diffusing AMPARs, potentially irrespective of their phosphorylation or other posttranslational modifications ( Diaz-Alonso et al., 2020 ).…”

Section: Discussionmentioning

confidence: 99%

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Sustained postsynaptic kainate receptor activation downregulates AMPA receptor surface expression and induces hippocampal LTD

et al. 2021

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Summary It is well established that long-term depression (LTD) can be initiated by either NMDA or mGluR activation. Here we report that sustained activation of GluK2 subunit-containing kainate receptors (KARs) leads to α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) endocytosis and induces LTD of AMPARs (KAR-LTD AMPAR ) in hippocampal neurons. The KAR-evoked loss of surface AMPARs is blocked by the ionotropic KAR inhibitor UBP 310 indicating that KAR-LTD AMPAR requires KAR channel activity. Interestingly, however, blockade of PKC or PKA also reduces GluA2 surface expression and occludes the effect of KAR activation. In acute hippocampal slices, kainate application caused a significant loss of GluA2-containing AMPARs from synapses and long-lasting depression of AMPAR excitatory postsynaptic currents in CA1. These data, together with our previously reported KAR-LTP AMPAR , demonstrate that KARs can bidirectionally regulate synaptic AMPARs and synaptic plasticity via different signaling pathways.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Sustained postsynaptic kainate receptor activation downregulates AMPA receptor surface expression and induces hippocampal LTD

et al. 2021

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“…LTP induces recruitment of AMPAR while LTD is accompanied by internalization of AMPAR ( Yuste and Bonhoeffer, 2001 ; Malinow and Malenka, 2002 ; Matsuzaki et al, 2004 ). In this regard, the necessity and sufficiency of GluA1 and GluA2 C-terminal domain for LTP and LTD, respectively with differential implications on spatial and contextual learning and memory has been recently reported ( Zhou et al, 2018 ) even if discrepancies regarding the requirement of C-terminal domain of GluA1 for LTP were reported by other authors (see Díaz-Alonso et al, 2020 ). GluA1 trafficking is strongly associated with LTP ( Lee et al, 2003 ; Makino and Malinow, 2009 ; Huganir and Nicoll, 2013 ) while GluA2 plays a prominent role in LTD ( Diering and Huganir, 2018 ).…”

Section: Memory Retrieval: An Ampar Storymentioning

confidence: 99%

AMPA Receptors: A Key Piece in the Puzzle of Memory Retrieval

Pereyra

Medina

2021

Front. Hum. Neurosci.

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Retrieval constitutes a highly regulated and dynamic phase in memory processing. Its rapid temporal scales require a coordinated molecular chain of events at the synaptic level that support transient memory trace reactivation. AMPA receptors (AMPAR) drive the majority of excitatory transmission in the brain and its dynamic features match the singular fast timescales of memory retrieval. Here we provide a review on AMPAR contribution to memory retrieval regarding its dynamic movements along the synaptic compartments, its changes in receptor number and subunit composition that take place in activity dependent processes associated with retrieval. We highlight on the differential regulations exerted by AMPAR subunits in plasticity processes and its impact on memory recall.

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“…The emergent roles of the GluA1 CTD in synaptic plasticity have been extensively documented (13,(15)(16)(17). However, the observation that the CTD-lacking GluA1 is still present at the postsynaptic membrane and mediates LTP (18,19) challenged the absolute requirement for GluA1 CTD in synaptic transmission and plasticity, indicating that other domains, such as the ATD, might have a previously uncovered role in LTP.…”

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confidence: 99%

The amino-terminal domain of GluA1 mediates LTP maintenance via interaction with neuroplastin-65

Jiang

Wei

Zhang

et al. 2021

Proc. Natl. Acad. Sci. U.S.A.

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Long-term potentiation (LTP) has long been considered as an important cellular mechanism for learning and memory. LTP expression involves NMDA receptor-dependent synaptic insertion of AMPA receptors (AMPARs). However, how AMPARs are recruited and anchored at the postsynaptic membrane during LTP remains largely unknown. In this study, using CRISPR/Cas9 to delete the endogenous AMPARs and replace them with the mutant forms in single neurons, we have found that the amino-terminal domain (ATD) of GluA1 is required for LTP maintenance. Moreover, we show that GluA1 ATD directly interacts with the cell adhesion molecule neuroplastin-65 (Np65). Neurons lacking Np65 exhibit severely impaired LTP maintenance, and Np65 deletion prevents GluA1 from rescuing LTP in AMPARs-deleted neurons. Thus, our study reveals an essential role for GluA1/Np65 binding in anchoring AMPARs at the postsynaptic membrane during LTP.

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Long-term potentiation is independent of the C-tail of the GluA1 AMPA receptor subunit

Cited by 32 publications

References 35 publications

Sustained postsynaptic kainate receptor activation downregulates AMPA receptor surface expression and induces hippocampal LTD

Sustained postsynaptic kainate receptor activation downregulates AMPA receptor surface expression and induces hippocampal LTD

AMPA Receptors: A Key Piece in the Puzzle of Memory Retrieval

The amino-terminal domain of GluA1 mediates LTP maintenance via interaction with neuroplastin-65

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