scholarly journals SUMOylation Is Required for Glycine-Induced Increases in AMPA Receptor Surface Expression (ChemLTP) in Hippocampal Neurons

PLoS ONE ◽  
2013 ◽  
Vol 8 (1) ◽  
pp. e52345 ◽  
Author(s):  
Nadia Jaafari ◽  
Filip A. Konopacki ◽  
Thomas F. Owen ◽  
Sriharsha Kantamneni ◽  
Philip Rubin ◽  
...  
Keyword(s):  
Ampa Receptor ◽  
Hippocampal Neurons ◽  
Surface Expression ◽  
Receptor Surface Expression

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

2020 ◽  
Author(s):  
Jithin D. Nair ◽  
Ellen Braksator ◽  
Busra P Yucel ◽  
Richard Seager ◽  
Jack R. Mellor ◽  
...  
Keyword(s):  
Ampa Receptor ◽  
Ampa Receptors ◽  
Hippocampal Neurons ◽  
Hippocampal Slices ◽  
Surface Expression ◽  
Receptor Activation ◽  
Kainate Receptors ◽  
Receptor Surface Expression ◽  
Acute Hippocampal Slices

AbstractHere we report that sustained activation of GluK2 subunit-containing kainate receptors leads to AMPA receptor endocytosis and a novel form of long-term depression (KAR-LTDAMPAR) in hippocampal neurons. The KAR-evoked loss of surface AMPA receptors requires KAR channel activity and is occluded by the blockade of PKC or PKA. Moreover, in acute hippocampal slices, kainate invoked LTD of AMPA EPSCs. These data, together with our previously reported KAR-LTPAMPAR, demonstrate that KARs bidirectionally regulate synaptic AMPARs and synaptic plasticity.

REGULATION OF AMPA RECEPTOR SURFACE EXPRESSION BY A NSF-DEPENDENT MECHANISM IN HIPPOCAMPAL NEURONS IN CULTURE

1999 ◽  
Vol 27 (3) ◽  
pp. A117-A117
Author(s):  
J. Noel ◽  
G. Scott Ralph ◽  
L. Pickard ◽  
E. Molnar ◽  
J. B. Uney ◽  
...  
Keyword(s):  
Ampa Receptor ◽  
Hippocampal Neurons ◽  
Surface Expression ◽  
Receptor Surface Expression ◽  
Dependent Mechanism

GRASP1 ubiquitination regulates AMPA receptor surface expression and synaptic activity in cultured hippocampal neurons

2021 ◽  
Vol 35 (8) ◽  
Author(s):  
Miranda Mele ◽  
Pasqualino De Luca ◽  
Ana Rita Santos ◽  
Marta Vieira ◽  
Ivan L. Salazar ◽  
...  
Keyword(s):  
Ampa Receptor ◽  
Hippocampal Neurons ◽  
Surface Expression ◽  
Synaptic Activity ◽  
Receptor Surface Expression ◽  
Cultured Hippocampal Neurons

scholarly journals Bidirectional Regulation of Kainate Receptor Surface Expression in Hippocampal Neurons

2008 ◽  
Vol 283 (52) ◽  
pp. 36435-36440 ◽  
Author(s):  
Stéphane Martin ◽  
Tristan Bouschet ◽  
Emma L. Jenkins ◽  
Atsushi Nishimune ◽  
Jeremy M. Henley
Keyword(s):  
Hippocampal Neurons ◽  
Surface Expression ◽  
Kainate Receptor ◽  
Bidirectional Regulation ◽  
Receptor Surface Expression

scholarly journals MicroRNA-186-5p controls GluA2 surface expression and synaptic scaling in hippocampal neurons

2019 ◽  
Vol 116 (12) ◽  
pp. 5727-5736 ◽  
Author(s):  
Mariline M. Silva ◽  
Beatriz Rodrigues ◽  
Joana Fernandes ◽  
Sandra D. Santos ◽  
Laura Carreto ◽  
...  
Keyword(s):  
Ampa Receptor ◽  
Ampa Receptors ◽  
Hippocampal Neurons ◽  
Surface Expression ◽  
Receptor Expression ◽  
Synaptic Activity ◽  
Synaptic Scaling ◽  
Posttranscriptional Control ◽  
Direct Target ◽  
Activity Dependent

Homeostatic synaptic scaling is a negative feedback response to fluctuations in synaptic strength induced by developmental or learning-related processes, which maintains neuronal activity stable. Although several components of the synaptic scaling apparatus have been characterized, the intrinsic regulatory mechanisms promoting scaling remain largely unknown. MicroRNAs may contribute to posttranscriptional control of mRNAs implicated in different stages of synaptic scaling, but their role in these mechanisms is still undervalued. Here, we report that chronic blockade of glutamate receptors of the AMPA and NMDA types in hippocampal neurons in culture induces changes in the neuronal mRNA and miRNA transcriptomes, leading to synaptic upscaling. Specifically, we show that synaptic activity blockade persistently down-regulates miR-186-5p. Moreover, we describe a conserved miR-186-5p-binding site within the 3′UTR of the mRNA encoding the AMPA receptor GluA2 subunit, and demonstrate that GluA2 is a direct target of miR-186-5p. Overexpression of miR-186 decreased GluA2 surface levels, increased synaptic expression of GluA2-lacking AMPA receptors, and blocked synaptic scaling, whereas inhibition of miR-186-5p increased GluA2 surface levels and the amplitude and frequency of AMPA receptor-mediated currents, and mimicked excitatory synaptic scaling induced by synaptic inactivity. Our findings elucidate an activity-dependent miRNA-mediated mechanism for regulation of AMPA receptor expression.

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