Integration of biochemical signalling in spines
Abstract
Short-term and long-term changes in the strength of synapses in neural networks underlie working memory and long-term memory storage in the brain. These changes are regulated by many biochemical signalling pathways in the postsynaptic spines of excitatory synapses. Recent findings about the roles and regulation of the small GTPases Ras, Rap and Rac in spines provide new insights into the coordination and cooperation of different pathways to effect synaptic plasticity. Here, we present an initial working representation of the interactions of five signalling cascades that are usually studied individually. We discuss their integrated function in the regulation of postsynaptic plasticity.
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Calcium ions in dendritic spines have an important function in activating signaling cascades that underlie and regulate synaptic plasticity.
“Calcium ions in dendritic spines have an important function in activating signaling cascades that underlie and regulate synaptic plasticity (Kennedy et al., 2005).”
From Barriers in the brain: resolving dendritic spine morphology and compartmentalization (2014) · cites this paper as Kennedy et al., 2005
The precise crosstalk and integration of Rho, Cdc42 and Rac is not completely understood.
“The precise crosstalk and integration is however not completely understood (Kennedy et al., 2005).”
From Barriers in the brain: resolving dendritic spine morphology and compartmentalization (2014) · cites this paper as Kennedy et al., 2005
SynGAP's broad action on dendritic spine signaling arises from its central location in the NMDAR complex and its promiscuous GAP domain that can regulate various small G-proteins.
“This broad action of SynGAP on dendritic spine signaling arises from its central location in the NMDAR complex (Kennedy et al., 2005) and its endowment with a promiscuous GAP domain that can regulate a variety of small G-proteins (Krapivinsky et al., 2004; Pena et al., 2008).”
From Pathogenic SYNGAP1 Mutations Impair Cognitive Development by Disrupting Maturation of Dendritic Spine Synapses (2012) · cites this paper as Kennedy et al., 2005
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- Authors
- Kennedy, M. B., Beale, H. C., Carlisle, H. J., & Washburn, L. R.
- Affiliations
- California Institute of Technology (US)
- Corresponding author
- Kennedy, Mary B.
- Venue
- Nature Reviews Neuroscience
- Published
- 2005-06-01
- Volume
- 6
- Issue
- 6
- Pages
- 423-434
- ISSN
- 1471-003X (ISSN-L)
- 1471-0048
- OpenAlex
- W2005797241
- Cited by
- 286
- References
- 127
- Citations by year
- 2025: 3 · 2024: 7 · 2023: 4 · 2022: 5 · 2021: 7 · 2020: 9 · 2019: 11 · 2018: 12 · 2017: 6 · 2016: 10 · 2015: 10 · 2014: 14 · 2013: 14 · 2012: 38
- FWCI
- 2.35
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Nature reviews. Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- CaltechAUTHORS (California Institute of Technology) (submittedVersion)
- Funders
- John Douglas French Alzheimer's Foundation
- National Institutes of Health
- National Institute on Drug Abuse (R01DA030749)
- National Institute of Neurological Disorders and Stroke (P01NS044306)
- 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
- postsynaptic spines, synaptic plasticity, Ras, rap, Rac, small GTPases, excitatory synapses, working memory, long-term memory, signaling pathways
- MeSH terms
- Animals, Humans, Neuronal Plasticity, Synapses, Signal Transduction, Calcium Signaling, Dendritic Spines
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