ArticleThe European journal of neuroscience2012
β3 integrin is dispensable for conditioned fear and hebbian forms of plasticity in the hippocampus.
Article in The European journal of neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- Itgb3 expression is developmentally regulated in pyramidal neurons of mouse cortex and hippocampus.Neuroscience letters · 2026Article
- Convergence and divergence of molecular mechanisms in Hebbian and homeostatic plasticity.Frontiers in synaptic neuroscience · 2026Review
- Dysregulated cortical excitability and tau phosphorylation in a β3 integrin mouse model of autism.Brain : a journal of neurology · 2025Article
- The Serine/Threonine Kinase NDR2 Regulates Integrin Signaling, Synapse Formation, and Synaptic Plasticity in the Hippocampus.Journal of neurochemistry · 2025Article
- Integrin β3 regulates apical dendritic morphology of pyramidal neurons throughout hippocampal CA3.Hippocampus · 2023Article
- Osteopontin/secreted phosphoprotein-1 harnesses glial-, immune-, and neuronal cell ligand-receptor interactions to sense and regulate acute and chronic neuroinflammation.Immunological reviews · 2022Review
- CRISPR-mediated activation of autism geneMolecular therapy. Nucleic acids · 2022Article
- Integrins Bidirectionally Regulate the Efficacy of Inhibitory Synaptic Transmission and Control GABAergic Plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Integrin β3 in forebrain Emx1-expressing cells regulates repetitive self-grooming and sociability in mice.BMC neuroscience · 2022Article
- CRISPR-Mediated Activation of αV Integrin Subtypes Promotes Neuronal Differentiation of Neuroblastoma Neuro2a Cells.Frontiers in genome editing · 2022Article
- Extracellular Matrix Signaling Through β3 Integrin Mediates Cocaine Cue-Induced Transient Synaptic Plasticity and Relapse.Biological psychiatry · 2019Article
- Intra- and Extracellular Pillars of a Unifying Framework for Homeostatic Plasticity: A Crosstalk Between Metabotropic Receptors and Extracellular Matrix.Frontiers in cellular neuroscience · 2019Review
- Integrins in synapse regulation.Nature reviews. Neuroscience · 2016Review
- Dopamine increases NMDA-stimulated calcium flux in striatopallidal neurons through a matrix metalloproteinase-dependent mechanism.The European journal of neuroscience · 2016Article
- Intercellular protein-protein interactions at synapses.Protein & cell · 2014Review
- ECM receptors in neuronal structure, synaptic plasticity, and behavior.Progress in brain research · 2014Review
- Cell biology in neuroscience: the interplay between Hebbian and homeostatic synaptic plasticity.The Journal of cell biology · 2013Review
- Mice lacking integrin β3 expression exhibit altered response to chronic stress.Neurobiology of stressArticle
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Integrins play key roles in the developing and mature nervous system, from promoting neuronal process outgrowth to facilitating synaptic plasticity. Recently, in hippocampal pyramidal neurons, β3 integrin (ITGβ3) was shown to stabilise synaptic AMPA receptors (AMPARs) and to be required for homeostatic scaling of AMPARs elicited by chronic activity suppression. To probe the physiological function for ITGβ3-dependent processes in the brain, we examined whether the loss of ITGβ3 affected fear-related behaviours in mice. ITGβ3-knockout (KO) mice showed normal conditioned fear responses that were similar to those of control wild-type mice. However, anxiety-like behaviour appeared substantially compromised and could be reversed to control levels by lentivirus-mediated re-expression of ITGβ3 bilaterally in the ventral hippocampus. In hippocampal slices, the loss of ITGβ3 activity did not compromise hebbian forms of plasticity--neither acute pharmacological disruption of ITGβ3 ligand interactions nor genetic deletion of ITGβ3 altered long-term potentiation (LTP) or long-term depression (LTD). Moreover, we did not detect any changes in short-term synaptic plasticity upon loss of ITGβ3 activity. In contrast, acutely disrupting ITGβ1-ligand interactions or genetic deletion of ITGβ1 selectively interfered with LTP stabilisation whereas LTD remained unaltered. These findings indicate a lack of requirement for ITGβ3 in the two robust forms of hippocampal long-term synaptic plasticity, LTP and LTD, and suggest differential roles for ITGβ1 and ITGβ3 in supporting hippocampal circuit functions.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.