Cited by 185Neuroscience and Neuropharmacology ResearchProtein Kinase Regulation and GTPase SignalingMemory and Neural Mechanisms

AKAP signaling complexes in regulation of excitatory synaptic plasticity

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Sanderson, Jennifer L., Dell'Acqua, Mark L.·2011·The Neuroscientist

Abstract

Plasticity at excitatory glutamatergic synapses in the central nervous system is believed to be critical for neuronal circuits to process and encode information, allowing animals to perform complex behaviors such as learning and memory. In addition, alterations in synaptic plasticity are associated with human diseases, including Alzheimer disease, epilepsy, chronic pain, drug addiction, and schizophrenia. Long-term potentiation (LTP) and depression (LTD) in the hippocampal region of the brain are two forms of synaptic plasticity that increase or decrease, respectively, the strength of synaptic transmission by postsynaptic AMPA-type glutamate receptors. Both LTP and LTD are induced by activation of NMDA-type glutamate receptors but differ in the level and duration of Ca 2+ influx through the NMDA receptor and the subsequent engagement of downstream signaling by protein kinases, including PKA, PKC, and CaMKII, and phosphatases, including PP1 and calcineurin-PP2B (CaN). This review addresses the important emerging roles of the A-kinase anchoring protein family of scaffold proteins in regulating localization of PKA and other kinases and phosphatases to postsynaptic multiprotein complexes that control NMDA and AMPA receptor function during LTP and LTD.

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  • AKAP5 anchors both PKA and CaN to GluA1, allowing for efficient coordination of these signaling pathways during LTD.

    “AKAP5 anchors both PKA and CaN to GluA1 allowing for the efficient coordination of these signaling pathways during LTD (Sanderson and Dell'Acqua, 2011).”

    From The AMPA Receptor Code of Synaptic Plasticity (2018) · cites this paper as Sanderson and Dell'Acqua, 2011

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  1. Malenka RC Bear MF LTP and LTD: an embarrassment of riches. Neuron 2004 44 1 5 21 15450156

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Authors
Sanderson, J. L., & Dell'Acqua, M. L.
Affiliations
  • University of Colorado Anschutz (US)
  • Department of Pharmacology, University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, CO, USA, Program in Neuroscience, University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, CO, USA,
Venue
The Neuroscientist
Published
2011-04-15
Volume
17
Issue
3
Pages
321-336
ISSN
  • 1073-8584 (ISSN-L)
  • 1089-4098
OpenAlex
W2126128061
Cited by
185
References
89
Citations by year
2026: 6 · 2025: 7 · 2024: 12 · 2023: 7 · 2022: 9 · 2021: 8 · 2020: 4 · 2019: 9 · 2018: 8 · 2017: 12 · 2016: 16 · 2015: 24 · 2014: 23 · 2013: 20 · 2012: 17
FWCI
1.92
Type
journal article
Language
en
Open access
Locations
  • The Neuroscientist (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institute on Alcohol Abuse and Alcoholism (T32AA007464)
  • National Institute of Mental Health (R01MH080291)
  • National Institute of Neurological Disorders and Stroke (R01NS040701)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
Keywords
A-kinase anchoring proteins, synaptic plasticity, long-term potentiation, long-term depression, NMDA receptor, AMPA receptors, calcium/calmodulin-dependent protein kinase II, protein kinase A, protein kinase C, calcineurin, scaffold proteins, hippocampus, glutamatergic synapses
MeSH terms
Animals, Brain, Humans, Synaptic Transmission, Neuronal Plasticity, Signal Transduction, A Kinase Anchor Proteins

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