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

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AKAP Signaling Complexes in Regulation of Excitatory Synaptic Plasticity

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

DOI 10.1177/1073858410384740PMC PMC3126619

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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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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,
ORCID: Sanderson, Jennifer L.
Venue: The Neuroscientist
Publisher: SAGE Publications
Published: 2011-04-15
Volume: 17
Issue: 3
Pages: 321-336
ISSN: 1073-8584 (ISSN-L)
1089-4098
DOI: 10.1177/1073858410384740
PMC: PMC3126619
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: green
www.ncbi.nlm.nih.gov
Licence: journals.sagepub.com/page/policies/text-and-data-mining-license (tdm)
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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AKAP Signaling Complexes in Regulation of Excitatory Synaptic Plasticity

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