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Mónica Fernández-Monreal

Researcher at Spanish National Research Council

Publications -  5
Citations -  307

Mónica Fernández-Monreal is an academic researcher from Spanish National Research Council. The author has contributed to research in topics: Synaptic plasticity & AMPA receptor. The author has an hindex of 5, co-authored 5 publications receiving 277 citations.

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PIP3 controls synaptic function by maintaining AMPA receptor clustering at the postsynaptic membrane

TL;DR: It is shown that continuous synthesis and availability of phosphatidylinositol-(3,4,5)-trisphosphate at the postsynaptic terminal is necessary for sustaining synaptic function in rat hippocampal neurons, specific for synaptic, but not extrasynaptic, AMPA receptors, nor for NMDA receptors.
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The Balance between Receptor Recycling and Trafficking toward Lysosomes Determines Synaptic Strength during Long-Term Depression

TL;DR: The functional contribution of receptor recycling versus degradation for LTD in rat hippocampal slices, and their correlation with receptor dephosphorylation is examined, contributing to clarify the fate of AMPARs during LTD and emphasize the importance of membrane sorting decisions to determine the outcome of synaptic plasticity.
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Tissue Plasminogen Activator Alters Intracellular Sequestration of Zinc through Interaction with the Transporter ZIP4

TL;DR: It is shown that ZIP4 is upregulated after excitotoxin stimulation of the mouse, male and female, hippocampus, and changes in prosurvival signals support the idea that this sequestration results in neuroprotection.
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APPL1 gates long-term potentiation through its plekstrin homology domain.

TL;DR: How a trafficking protein, APPL1, mediates synaptic plasticity events depending on the involvement of PI3K intracellular signaling, rather than on the outcome of the synaptic change (potentiation versus depression).
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A retention–release mechanism based on RAB11FIP2 for AMPA receptor synaptic delivery during long-term potentiation

TL;DR: Surprisingly, it is found that FIP2 operates independently from Rab11 proteins, and acts as a negative regulator of AMPAR synaptic trafficking, and is proposed as a retention–release mechanism that restricts the trafficking of AMPA receptors until LTP induction triggers their release and allows synaptic delivery.