Cortical development of AMPA receptor trafficking proteins
Open accessAbstract
AMPA-receptor trafficking plays a central role in excitatory plasticity, especially during development. Changes in the number of AMPA receptors and time spent at the synaptic surface are important factors of plasticity that directly affect long-term potentiation (LTP), long-term depression (LTD), synaptic scaling, and the excitatory-inhibitory (E/I) balance in the developing cortex. Experience-dependent changes in synaptic strength in visual cortex (V1) use a molecularly distinct AMPA trafficking pathway that includes the GluA2 subunit. We studied developmental changes in AMPA receptor trafficking proteins by quantifying expression of GluA2, pGluA2 (GluA2serine880), GRIP1, and PICK1 in rat visual and frontal cortex. We used Western Blot analysis of synaptoneurosome preparations of rat visual and frontal cortex from animals ranging in age from P0 to P105. GluA2 and pGluA2 followed different developmental trajectories in visual and frontal cortex, with a brief period of over expression in frontal cortex. The over expression of GluA2 and pGluA2 in immature frontal cortex raises the possibility that there may be a period of GluA2-dependent vulnerability in frontal cortex that is not found in V1. In contrast, GRIP1 and PICK1 had the same developmental trajectories and were expressed very early in development of both cortical areas. This suggests that the AMPA-interacting proteins are available to begin trafficking receptors as soon as GluA2-containing receptors are expressed. Finally, we used all four proteins to analyze the surface-to-internalization balance and found that this balance was roughly equal across both cortical regions, and throughout development. Our finding of an exquisite surface-to-internalization balance highlights that these AMPA receptor trafficking proteins function as a tightly controlled system in the developing cortex.
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In rats, AMPA/Kainate receptor binding sites and GluR2 protein begin to decline between ~P24-P30 and P60.
“In rats, AMPA/Kainate receptor binding sites (Insel et al., 1990) and GluR2 protein (Murphy et al., 2012) begin to decline between ~P24-P30 and P60.”
From Does puberty mark a transition in sensitive periods for plasticity in the associative neocortex? (2017) · cites this paper as Murphy et al., 2012
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- Authors
- Murphy, K. M., Tcharnaia, L., Beshara, S. P., & Jones, D. G.
- Affiliations
- McMaster University (CA)
- Corresponding author
- Murphy, Kathryn M.
- ORCID
- Murphy, Kathryn M.
- Venue
- Frontiers in Molecular Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2012
- Volume
- 5
- Pages
- 65-65
- ISSN
- 1662-5099 (ISSN-L)
- PMC
- PMC3353264
- OpenAlex
- W1993609022
- Cited by
- 20
- References
- 58
- Citations by year
- 2025: 3 · 2024: 3 · 2023: 1 · 2022: 1 · 2020: 2 · 2018: 3 · 2016: 1 · 2015: 2 · 2014: 1 · 2013: 3
- FWCI
- 0.79
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by-nc
- Locations
- Frontiers in Molecular Neuroscience (publishedVersion, cc-by-nc)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- 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 › Molecular Biology › Receptor Mechanisms and Signaling
- Keywords
- AMPA receptor trafficking, GluA2, GRIP1, PICK1, cortical development, visual cortex, frontal cortex, synaptic scaling, excitation-inhibition balance, receptor internalization, synaptoneurosomes, long-term potentiation, long-term depression
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