Pathophysiology of locus ceruleus neurons in a mouse model of Rett syndrome - Test2 - elhamkhani - TriplyDB

Pathophysiology of locus ceruleus neurons in a mouse model of Rett syndrome

Pathophysiology of locus ceruleus neurons in a mouse model of Rett syndrome

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Loss of MeCP2 in aminergic neurons causes cell-autonomous defects in neurotransmitter synthesis and specific behavioral abnormalities Rett Syndrome: Crossing the Threshold to Clinical Translation MECP2 disorders: from the clinic to mice and back GABA and glutamate pathways are spatially and developmentally affected in the brain of Mecp2-deficient mice Characterization of Rett Syndrome-like phenotypes in Mecp2-knockout rats Brain activity mapping in Mecp2 mutant mice reveals functional deficits in forebrain circuits, including key nodes in the default mode network, that are reversed with ketamine treatment.Network hyperexcitability in hippocampal slices from Mecp2 mutant mice revealed by voltage-sensitive dye imaging.Morphological and functional reversal of phenotypes in a mouse model of Rett syndrome.Preclinical research in Rett syndrome: setting the foundation for translational success.mTORC1 Is a Local, Postsynaptic Voltage Sensor Regulated by Positive and Negative Feedback Pathways.The neural circuit basis of Rett syndrome Biogenic amines and their metabolites are differentially affected in the Mecp2-deficient mouse brain.β2-Adrenergic receptor agonist ameliorates phenotypes and corrects microRNA-mediated IGF1 deficits in a mouse model of Rett syndrome Pontine norepinephrine defects in Mecp2-null mice involve deficient expression of dopamine beta-hydroxylase but not a loss of catecholaminergic neurons.The locus coeruleus and central chemosensitivity Alterations in the cholinergic system of brain stem neurons in a mouse model of Rett syndrome Experimental models of Rett syndrome based on Mecp2 dysfunction.Chronic alterations in monoaminergic cells in the locus coeruleus in orexin neuron-ablated narcoleptic mice Complexities of Rett syndrome and MeCP2 Network models predict that reduced excitatory fluctuations can give rise to hippocampal network hyper-excitability in MeCP2-null mice The disruption of central CO2 chemosensitivity in a mouse model of Rett syndrome.MECP2e1 isoform mutation affects the form and function of neurons derived from Rett syndrome patient iPS cells.Synaptic microcircuit dysfunction in genetic models of neurodevelopmental disorders: focus on Mecp2 and Met.Loss of Mecp2 in substantia nigra dopamine neurons compromises the nigrostriatal pathway.Methyl CpG Binding Protein 2 Gene Disruption Augments Tonic Currents of γ-Aminobutyric Acid Receptors in Locus Coeruleus Neurons: IMPACT ON NEURONAL EXCITABILITY AND BREATHING.Engrailed-2 (En2) deletion produces multiple neurodevelopmental defects in monoamine systems, forebrain structures and neurogenesis and behavior Decreased Hering-Breuer input-output entrainment in a mouse model of Rett syndrome.GABAergic synaptic inputs of locus coeruleus neurons in wild-type and Mecp2-null mice.Identification of clinical target areas in the brainstem of prion-infected mice.Neuronal morphology in MeCP2 mouse models is intrinsically variable and depends on age, cell type, and Mecp2 mutation.Breathing challenges in Rett syndrome: lessons learned from humans and animal models.Reduced neuronal size and mTOR pathway activity in the Mecp2 A140V Rett syndrome mouse model Pre- and postsynaptic modulations of hypoglossal motoneurons by α-adrenoceptor activation in wild-type and Mecp2(-/Y) mice Effects of early-life exposure to THIP on phenotype development in a mouse model of Rett syndrome.When norepinephrine becomes a driver of breathing irregularities: how intermittent hypoxia fundamentally alters the modulatory response of the respiratory network.Rescue of behavioral and EEG deficits in male and female Mecp2-deficient mice by delayed Mecp2 gene reactivation.Negative Allosteric Modulation of mGluR5 Partially Corrects Pathophysiology in a Mouse Model of Rett Syndrome.Loss of MeCP2 from forebrain excitatory neurons leads to cortical hyperexcitation and seizures.Effects of early-life exposure to THIP on brainstem neuronal excitability in the Mecp2-null mouse model of Rett syndrome before and after drug withdrawal.Functional neuroanatomy of the central noradrenergic system.

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Pathophysiology of locus ceruleus neurons in a mouse model of Rett syndrome

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Pathophysiology of locus ceruleus neurons in a mouse model of Rett syndrome

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Pathophysiology of locus ceruleus neurons in a mouse model of Rett syndrome

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Pathophysiology of locus ceruleus neurons in a mouse model of Rett syndrome

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Pathophysiology of locus ceruleus neurons in a mouse model of Rett syndrome

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Pathophysiology of locus ceruleus neurons in a mouse model of Rett syndrome

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Pathophysiology of locus ceruleus neurons in a mouse model of Rett syndrome

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Pathophysiology of locus ceruleus neurons in a mouse model of Rett syndrome

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Danielle A Schmid

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David M Katz

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Gabriel Brooks-Harris

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Michael Ogier

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Praveen Taneja

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P2860

Rett syndrome is caused by mutations in X-linked MECP2, encoding methyl-CpG-binding protein 2

Autism, fever, epigenetics and the locus coeruleus

Reduced cortical activity due to a shift in the balance between excitation and inhibition in a mouse model of Rett syndrome

The story of Rett syndrome: from clinic to neurobiology

Learning and memory and synaptic plasticity are impaired in a mouse model of Rett syndrome

MeCP2 controls excitatory synaptic strength by regulating glutamatergic synapse number

Defect in normal developmental increase of the brain biogenic amine concentrations in the mecp2-null mouse

Mecp2 deficiency disrupts norepinephrine and respiratory systems in mice

MECP2 is progressively expressed in post-migratory neurons and is involved in neuronal maturation rather than cell fate decisions

Deficiency of methyl-CpG binding protein-2 in CNS neurons results in a Rett-like phenotype in mice

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