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Complete or partial reduction of the Met receptor tyrosine kinase in distinct circuits differentially impacts mouse behavior / B. L. THOMPSON in Journal of Neurodevelopmental Disorders, 7-1 (December 2015)
[article]
Titre : Complete or partial reduction of the Met receptor tyrosine kinase in distinct circuits differentially impacts mouse behavior Type de document : Texte imprimé et/ou numérique Auteurs : B. L. THOMPSON, Auteur ; P. LEVITT, Auteur Article en page(s) : p.35 Langues : Anglais (eng) Mots-clés : Autism Behavior Fear learning Gene dose Met Mouse Phenotype Index. décimale : PER Périodiques Résumé : BACKGROUND: Our 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. METHODS: Mating 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. RESULTS: Met (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. CONCLUSIONS: These 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. En ligne : http://dx.doi.org/10.1186/s11689-015-9131-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=348
in Journal of Neurodevelopmental Disorders > 7-1 (December 2015) . - p.35[article] Complete or partial reduction of the Met receptor tyrosine kinase in distinct circuits differentially impacts mouse behavior [Texte imprimé et/ou numérique] / B. L. THOMPSON, Auteur ; P. LEVITT, Auteur . - p.35.
Langues : Anglais (eng)
in Journal of Neurodevelopmental Disorders > 7-1 (December 2015) . - p.35
Mots-clés : Autism Behavior Fear learning Gene dose Met Mouse Phenotype Index. décimale : PER Périodiques Résumé : BACKGROUND: Our 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. METHODS: Mating 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. RESULTS: Met (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. CONCLUSIONS: These 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. En ligne : http://dx.doi.org/10.1186/s11689-015-9131-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=348 Mice with Impaired Met Tyrosine Kinase Signaling Demonstrate Characteristics Relevant to Autism / Jacob M. SMITH in Autism - Open Access, 2-S ([01/12/2012])
[article]
Titre : Mice with Impaired Met Tyrosine Kinase Signaling Demonstrate Characteristics Relevant to Autism Type de document : Texte imprimé et/ou numérique Auteurs : Jacob M. SMITH, Auteur ; Elizabeth M. POWELL, Auteur Article en page(s) : 8 p. Langues : Anglais (eng) Mots-clés : HGF MET Interneuron Forebrain Attentional set-shifting Reversal learning Seizure Plaur Index. décimale : PER Périodiques Résumé : Variants of MET, a receptor tyrosine kinase which binds the ligand Hepatocyte growth factor (HGF), have been linked to elevated risk for developing autism spectrum disorders (ASD) in humans. Though best known as a proto-oncogene, MET also plays important roles during normal development, including the development of the central nervous system. Recent studies in several mouse lines have shown that mice with reduced HGF-Met signaling have altered profiles of interneurons in the cortex, striatum, and hippocampus. Alterations in neuronal development, particularly in the cerebral cortex, may contribute to the pathology of developmental disorders, including autism. Other studies have shown changes in excitatory signaling in the Met-deficient cortex. Interestingly, mice with deficient Met signaling also show behavioral alterations characteristic of autism. Here we review anatomical and behavioral findings in mice with altered HGF - Met signaling. En ligne : https://dx.doi.org/10.4172/2165-7890.S1-002 ER - Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=409
in Autism - Open Access > 2-S [01/12/2012] . - 8 p.[article] Mice with Impaired Met Tyrosine Kinase Signaling Demonstrate Characteristics Relevant to Autism [Texte imprimé et/ou numérique] / Jacob M. SMITH, Auteur ; Elizabeth M. POWELL, Auteur . - 8 p.
Langues : Anglais (eng)
in Autism - Open Access > 2-S [01/12/2012] . - 8 p.
Mots-clés : HGF MET Interneuron Forebrain Attentional set-shifting Reversal learning Seizure Plaur Index. décimale : PER Périodiques Résumé : Variants of MET, a receptor tyrosine kinase which binds the ligand Hepatocyte growth factor (HGF), have been linked to elevated risk for developing autism spectrum disorders (ASD) in humans. Though best known as a proto-oncogene, MET also plays important roles during normal development, including the development of the central nervous system. Recent studies in several mouse lines have shown that mice with reduced HGF-Met signaling have altered profiles of interneurons in the cortex, striatum, and hippocampus. Alterations in neuronal development, particularly in the cerebral cortex, may contribute to the pathology of developmental disorders, including autism. Other studies have shown changes in excitatory signaling in the Met-deficient cortex. Interestingly, mice with deficient Met signaling also show behavioral alterations characteristic of autism. Here we review anatomical and behavioral findings in mice with altered HGF - Met signaling. En ligne : https://dx.doi.org/10.4172/2165-7890.S1-002 ER - Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=409