PICK1 loss of function occludes homeostatic synaptic scaling
Open accessAbstract
Homeostatic synaptic scaling calibrates neuronal excitability by adjusting synaptic strengths during prolonged changes in synaptic activity. The molecular mechanisms that regulate the trafficking of AMPA receptors (AMPARs) during synaptic scaling are largely unknown. Here, we show that chronic activity blockade reduces PICK1 protein level on a time scale that coincides with the accumulation of surface AMPARs. PICK1 loss of function alters the subunit composition and the abundance of GluA2-containing AMPARs. Due to aberrant trafficking of these receptors, the increase in synaptic strength in response to synaptic inactivity is occluded in neurons generated from PICK1 knock-out mouse. In agreement with electrophysiological recordings, no defect of AMPAR trafficking is observed in PICK1 knock-out neurons in response to elevated neuronal activity. Overall, our data reveal an important role of PICK1 in inactivity-induced synaptic scaling by regulating the subunit composition, abundance, and trafficking of GluA2-containing AMPARs.
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Neither GRIP1/2 nor PICK1 are required for scaling-down.
“Neither GRIP1/2 nor PICK1 are required for scaling-down (Tan et al., 2015, Anggono et al., 2011).”
From The AMPA Receptor Code of Synaptic Plasticity (2018) · cites this paper as Anggono et al., 2011
The Results report robust scaling-down after bicuculline treatment in PICK1 knockout neurons, supporting the PICK1 part of the sentence. The cited paper does not establish that GRIP1/2 are dispensable for scaling-down, so it does not support the full claim attributed jointly to the two citations. (LLM, conf=0.84)
Experimental — accuracy not yet measuredProlonged TTX treatment in cultured neurons causes lysosomal degradation of PICK1, while deletion of PICK1 enhances mEPSC amplitude and occludes homeostatic scaling-up.
“Prolonged TTX treatment in cultured neurons causes lysosomal degradation of PICK1, while deletion of PICK1 enhances mEPSC amplitude and occludes homeostatic scaling-up, suggesting that decreased activity of PICK1 is an important mediator of scaling-up (Figure 3) (Anggono et al., 2011).”
From The AMPA Receptor Code of Synaptic Plasticity (2018) · cites this paper as Anggono et al., 2011
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Формы и механизмы гомеостатической синаптической пластичности
Novgorod, N., & Russian Federation (2013)
- Authors
- Anggono, V., Clem, R. L., & Huganir, R. L.
- Affiliations
- Howard Hughes Medical Institute (US)
- Corresponding author
- Huganir, Richard L.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2011-02-09
- Volume
- 31
- Issue
- 6
- Pages
- 2188-2196
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC3071039
- OpenAlex
- W2021088263
- Cited by
- 111
- References
- 43
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 1 · 2023: 5 · 2022: 3 · 2021: 4 · 2020: 6 · 2019: 11 · 2018: 10 · 2017: 10 · 2016: 8 · 2015: 10 · 2014: 10 · 2013: 14 · 2012: 10
- FWCI
- 4.90
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Howard Hughes Medical Institute
- Johns Hopkins University
- National Institutes of Health
- Medical Research Council
- National Health and Medical Research Council (477108)
- National Institute of Mental Health (F32MH087037)
- National Institute of Neurological Disorders and Stroke (R01NS036715)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Amino Acid Enzymes and Metabolism
- Keywords
- PICK1, homeostatic synaptic scaling, AMPA receptor trafficking, GluA2, AMPA receptor subunit composition, neuronal excitability, synaptic homeostasis
- MeSH terms
- Animals, Bicuculline, Carrier Proteins, Cells, Cultured, Cerebral Cortex, Embryo, Mammalian, Gene Expression Regulation, Homeostasis, Humans, Mice, Inbred C57BL, Neuronal Plasticity, Neurons, Nuclear Proteins, Synapses, Tetrodotoxin, Transfection, Receptors, AMPA, Mice, Knockout, Statistics, Nonparametric, Cell Cycle Proteins, Excitatory Postsynaptic Potentials, Biotinylation, Protein Subunits, Protein Transport, Sodium Channel Blockers, RNA, Small Interfering, Green Fluorescent Proteins, Mice, GABA-A Receptor Antagonists
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