ArticleThe Journal of comparative neurology2013
Synaptic and extrasynaptic location of the receptor tyrosine kinase met during postnatal development in the mouse neocortex and hippocampus.
Article in The Journal of comparative neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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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
28 citing papers in PubMed, 34 citations in OpenAlex.
- Alterations in the Proteome of Developing Neocortical Synaptosomes in the Absence of MET Signaling Revealed by Comparative Proteomics.Developmental neuroscience · 2023Article
- Disrupted Timing of MET Signaling Derails the Developmental Maturation of Cortical Circuits and Leads to Altered Behavior in Mice.Cerebral cortex (New York, N.Y. : 1991) · 2022Article
- Reduced HGF/MET Signaling May Contribute to the Synaptic Pathology in an Alzheimer's Disease Mouse Model.Frontiers in aging neuroscience · 2022Article
- Conditional knockout of MET receptor tyrosine kinase in cortical excitatory neurons leads to enhanced learning and memory in young adult mice but early cognitive decline in older adult mice.Neurobiology of learning and memory · 2021Article
- Distribution and localization of phosphatidylinositol 5-phosphate, 4-kinase alpha and beta in the brain.The Journal of comparative neurology · 2021Article
- HGF and MET: From Brain Development to Neurological Disorders.Frontiers in cell and developmental biology · 2021Review
- Autism Spectrum Disorder Risk Factor Met Regulates the Organization of Inhibitory Synapses.Frontiers in molecular neuroscience · 2021Article
- Control of cortical synapse development and plasticity by MET receptor tyrosine kinase, a genetic risk factor for autism.Journal of neuroscience research · 2020Review
- Article
- Semaphorin4D Induces Inhibitory Synapse Formation by Rapid Stabilization of Presynaptic Boutons via MET Coactivation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Precision in the development of neocortical architecture: From progenitors to cortical networks.Progress in neurobiology · 2019Review
- Amphetamine-induced Conditioned Place Preference and Changes in mGlu1/5 Receptor Expression and Signaling in the Rat Medial Prefrontal Cortex.Neuroscience · 2019Article
- Disruption of MET Receptor Tyrosine Kinase, an Autism Risk Factor, Impairs Developmental Synaptic Plasticity in the Hippocampus.Developmental neurobiology · 2019Article
- Alterations in mGlu5 receptor expression and function in the striatum in a rat depression model.Journal of neurochemistry · 2018Article
- Differential impact ofNeurobiology of stress · 2018Article
- Distinct projection targets define subpopulations of mouse brainstem vagal neurons that express the autism-associated MET receptor tyrosine kinase.The Journal of comparative neurology · 2017Article
- The Pleiotropic MET Receptor Network: Circuit Development and the Neural-Medical Interface of Autism.Biological psychiatry · 2017Review
- Receptor Tyrosine Kinase MET Interactome and Neurodevelopmental Disorder Partners at the Developing Synapse.Biological psychiatry · 2016Article
- Distinct intracellular signaling mediates C-MET regulation of dendritic growth and synaptogenesis.Developmental neurobiology · 2016Article
- The autism-associated MET receptor tyrosine kinase engages early neuronal growth mechanism and controls glutamatergic circuits development in the forebrain.Molecular psychiatry · 2016Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
MET, a replicated autism risk gene, encodes a pleiotropic receptor tyrosine kinase implicated in multiple cellular processes during development and following injury. Previous studies suggest that Met modulates excitatory synapse development in the neocortex and hippocampus, although the underlying mechanism is unknown. The peak of Met expression corresponds to the period of process outgrowth and synaptogenesis, with robust expression in hippocampal and neocortical neuropil. Resolving whether neuropil expression represents presynaptic, postsynaptic or glial localization provides insight into potential mechanisms of Met action. The subcellular distribution of Met was characterized using complementary ultrastructural, in situ proximity ligation assay (PLA), and biochemical approaches. At postnatal day (P) 7, immunoelectron microscopy revealed near-equivalent proportions of Met-immunoreactive pre- (axons and terminals) and postsynaptic (dendritic shafts and spines) profiles in the stratum radiatum in the hippocampal CA1 region. Staining was typically in elements in which the corresponding pre- or postsynaptic apposition was unlabeled. By P21, Met-immunoreactive presynaptic profiles predominated and ~20% of Met-expressing profiles were glial. A different distribution of Met-immunoreactive profiles was observed in layer V of somatosensory cortex: Met-labeled spines were rare and a smaller proportion of glial profiles expressed Met. Strikingly, Met-immunoreactive presynaptic profiles predominated over postsynaptic profiles as early as P7. PLA analysis of neurons in vitro and biochemical analysis of tissue subsynaptic fractions confirmed the localization of Met in specific synaptic subcompartments. The study demonstrates that Met is enriched at synapses during development and its activation may modulate synapse formation and stability through both pre- and postsynaptic mechanisms.
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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.