ArticleiScience2020
Pi4KIIα Regulates Unconditioned Stimulus-Retrieval-Induced Fear Memory Reconsolidation through Endosomal Trafficking of AMPA Receptors.
Article in iScience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- A ventral hippocampus-basolateral amygdala circuit regulates the unconditioned stimulus retrieval-induced reconsolidation of remote fear memory.Journal of advanced research · 2026Article
- Advances in fear memory erasure and its neural mechanisms.Frontiers in neurology · 2024Review
- Depression, anxiety, and burnout among psychiatrists during the COVID-19 pandemic: a cross-sectional study in Beijing, China.BMC psychiatry · 2023Article
- AKT and MAPK signaling pathways in hippocampus reveals the pathogenesis of depression in four stress-induced models.Translational psychiatry · 2023Article
- (2R,6R)-hydroxynorketamine acts through GluA1-induced synaptic plasticity to alleviate PTSD-like effects in rat models.Neurobiology of stress · 2022Article
- GSK-3β regulates the synaptic expression of NMDA receptors via phosphorylation of phosphatidylinositol 4 kinase type IIα.The European journal of neuroscience · 2021Article
- Apparent reconsolidation interference without generalized amnesia.Progress in neuro-psychopharmacology & biological psychiatry · 2021Article
- AMPA Receptors: A Key Piece in the Puzzle of Memory Retrieval.Frontiers in human neuroscience · 2021Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Targeting memory reconsolidation is an effective intervention for treating posttraumatic stress disorder (PTSD). Disrupting unconditioned stimulus (US)-retrieval-induced fear memory reconsolidation has become an effective therapeutic approach to attenuate fear memory, but the underlying molecular mechanisms remain unknown. Here, we report that US-retrieval-dependent increase in phosphatidylinositol 4-kinase IIα (Pi4KIIα) promotes early endosomal trafficking of AMPA receptors, leading to the enhancement of synaptic efficacy in basolateral amygdala (BLA) neurons. The inhibition of Pi4KIIα by an inhibitor or short hairpin RNA impaired contextual fear memory reconsolidation. This disruptive effect persisted for at least 2 weeks, which was restored by Pi4KIIα overexpression with TAT-Pi4KIIα. Furthermore, the blockade of early endosomal trafficking following US retrieval reduced synaptosomal membrane GluA1 levels and decreased subsequent fear expression. These data demonstrate that Pi4KIIα in the BLA is crucial for US-retrieval-induced fear memory reconsolidation, the inhibition of which might be an effective therapeutic strategy for treating PTSD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.