ArticleJournal of neurodevelopmental disorders2015
Complete or partial reduction of the Met receptor tyrosine kinase in distinct circuits differentially impacts mouse behavior.
Article in Journal of neurodevelopmental disorders, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 23 citations in OpenAlex.
- Developmental and molecular contributions to contextual fear memory emergence in mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Article
- Subclass-specific expression patterns of MET receptor tyrosine kinase during development in medial prefrontal and visual cortices.The Journal of comparative neurology · 2023Article
- Alterations in the Proteome of Developing Neocortical Synaptosomes in the Absence of MET Signaling Revealed by Comparative Proteomics.Developmental neuroscience · 2023Article
- Translational Magnetic Resonance Imaging in Autism Spectrum Disorder From the Mouse Model to Human.Frontiers in neuroscience · 2022Review
- Time-delimited signaling of MET receptor tyrosine kinase regulates cortical circuit development and critical period plasticity.Molecular psychiatry · 2021Article
- 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
- Control of cortical synapse development and plasticity by MET receptor tyrosine kinase, a genetic risk factor for autism.Journal of neuroscience research · 2020Review
- Cyclic Peptide-Based Biologics Regulating HGF-MET.International journal of molecular sciences · 2020Review
- Spaced training improves learning in Ts65Dn and Ube3a mouse models of intellectual disabilities.Translational psychiatry · 2019Article
- Disruption of MET Receptor Tyrosine Kinase, an Autism Risk Factor, Impairs Developmental Synaptic Plasticity in the Hippocampus.Developmental neurobiology · 2019Article
- Quantitative trait locus mapping and analysis of heritable variation in affiliative social behavior and co-occurring traits.Genes, brain, and behavior · 2018Article
- Altered synaptic transmission and maturation of hippocampal CA1 neurons in a mouse model of human chr16p11.2 microdeletion.Journal of neurophysiology · 2018Article
- Differential impact ofNeurobiology of stress · 2018Article
- Biological roles of hepatocyte growth factor-Met signaling from genetically modified animals.Biomedical reports · 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
- Early-Life Stress Paradigm Transiently Alters Maternal Behavior, Dam-Pup Interactions, and Offspring Vocalizations in Mice.Frontiers in behavioral neuroscience · 2016Article
- Altered Forebrain Functional Connectivity and Neurotransmission in a Kinase-Inactive Met Mouse Model of Autism.Molecular imagingArticle
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundOur laboratory discovered that the gene encoding the receptor tyrosine kinase, MET, contributes to autism risk. Expression of MET is reduced in human postmortem temporal lobe in autism and Rett Syndrome. Subsequent studies revealed a role for MET in human and mouse functional and structural cortical connectivity. To further understand the contribution of Met to brain development and its impact on behavior, we generated two conditional mouse lines in which Met is deleted from select populations of central nervous system neurons. Mice were then tested to determine the consequences of disrupting Met expression.
methodsMating of Emx1 (cre) and Met (fx/fx) mice eliminates receptor signaling from all cells arising from the dorsal pallium. Met (fx/fx) and Nestin (cre) crosses result in receptor signaling elimination from all neural cells. Behavioral tests were performed to assess cognitive, emotional, and social impairments that are observed in multiple neurodevelopmental disorders and that are in part subserved by circuits that express Met.
resultsMet (fx/fx) /Emx1 (cre) null mice displayed significant hypoactivity in the activity chamber and in the T-maze despite superior performance on the rotarod. Additionally, these animals showed a deficit in spontaneous alternation. Surprisingly, Met (fx/fx; fx/+) /Nestin (cre) null and heterozygous mice exhibited deficits in contextual fear conditioning, and Met (fx/+) /Nestin (cre) heterozygous mice spent less time in the closed arms of the elevated plus maze.
conclusionsThese data suggest a complex contribution of Met in the development of circuits mediating social, emotional, and cognitive behavior. The impact of disrupting developmental Met expression is dependent upon circuit-specific deletion patterns and levels of receptor activity.
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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.