ArticleMolecular neurobiology2017
GSK-3β and MMP-9 Cooperate in the Control of Dendritic Spine Morphology.
Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 45 citations in OpenAlex.
- Acute and reversible dyskinesias secondary to lithium toxicity: case report and literature review.BMC neurology · 2025Review
- Stress resilience is an active and multifactorial process manifested by structural, functional, and molecular changes in synapses.Neurobiology of stress · 2024Article
- Inhibition of GSK3α,β rescues cognitive phenotypes in a preclinical mouse model of CTNNB1 syndrome.EMBO molecular medicine · 2024Article
- Elevated matrix Metalloproteinase-9 associated with reduced cerebellar perineuronal nets in female mice with toxoplasmosis.Brain, behavior, & immunity - health · 2024Article
- Review
- The association of matrix metalloproteinase 9 (MMP9) with hippocampal volume in schizophrenia: a preliminary MRI study.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2022Article
- Molecular signature of extracellular matrix pathology in schizophrenia.The European journal of neuroscience · 2021Article
- GSK-3 Inhibition Modulates Metalloproteases in a Model of Lung Inflammation and Fibrosis.Frontiers in molecular biosciences · 2021Article
- GSK-3α/β Activity Negatively Regulates MMP-1/9 Expression to SuppressFrontiers in immunology · 2021Article
- TestingFrontiers in molecular neuroscience · 2021Article
- Changes in Gene and Protein Expression of Metalloproteinase-2 and -9 and Their Inhibitors TIMP2 and TIMP3 in Different Parts of Fluoride-Exposed Rat Brain.International journal of molecular sciences · 2020Article
- Matrix Metalloproteinase-9 Overexpression Regulates Hippocampal Synaptic Plasticity and Decreases Alcohol Consumption and Preference in Mice.Neurochemical research · 2020Article
- Preventive Electroacupuncture Ameliorates D-Galactose-Induced Alzheimer's Disease-Like Pathology and Memory Deficits Probably via Inhibition of GSK3Evidence-based complementary and alternative medicine : eCAM · 2020Article
- Ciliary neurotrophic factor signaling in the rat orbitofrontal cortex ameliorates stress-induced deficits in reversal learning.Neuropharmacology · 2019Article
- Loss of serum response factor in mature neurons in the dentate gyrus alters the morphology of dendritic spines and hippocampus-dependent behavioral tasks.Brain structure & function · 2019Article
- Decrease of GSK-3β Activity in the Anterior Cingulate Cortex ofFrontiers in cellular neuroscience · 2019Article
- GSK-3Neural plasticity · 2019Review
- GSK3β activity alleviates epileptogenesis and limits GluA1 phosphorylation.EBioMedicine · 2019Article
- DIXDC1 contributes to psychiatric susceptibility by regulating dendritic spine and glutamatergic synapse density via GSK3 and Wnt/β-catenin signaling.Molecular psychiatry · 2018Article
- Dcf1 Triggers Dendritic Spine Formation and Facilitates Memory Acquisition.Molecular neurobiology · 2018Article
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Changes in the morphology of dendritic spines are prominent during learning and in different neurological and neuropsychiatric diseases, including those in which glycogen synthase kinase-3β (GSK-3β) has been implicated. Despite much evidence of the involvement of GSK-3β in functional synaptic plasticity, it is unclear how GSK-3β controls structural synaptic plasticity (i.e., the number and shape of dendritic spines). In the present study, we used two mouse models overexpressing and lacking GSK-3β in neurons to investigate how GSK-3β affects the structural plasticity of dendritic spines. Following visualization of dendritic spines with DiI dye, we found that increasing GSK-3β activity increased the number of thin spines, whereas lacking GSK-3β increased the number of stubby spines in the dentate gyrus. Under conditions of neuronal excitation, increasing GSK-3β activity caused higher activity of extracellularly acting matrix metalloproteinase-9 (MMP-9), and MMP inhibition normalized thin spines in GSK-3β overexpressing mice. Administration of the nonspecific GSK-3β inhibitor lithium in animals with active MMP-9 and animals lacking MMP-9 revealed that GSK-3β and MMP-9 act in concert to control dendritic spine morphology. Altogether, our data demonstrate that the dysregulation of GSK-3β activity has dramatic consequences on dendritic spine morphology, implicating MMP-9 as a mediator of GSK-3β-induced synaptic alterations.
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