Altered NMDAR signaling underlies autistic-like features in mouse models of CDKL5 deficiency disorder
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Title
Altered NMDAR signaling underlies autistic-like features in mouse models of CDKL5 deficiency disorder
Authors
Keywords
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Journal
Nature Communications
Volume 10, Issue 1, Pages -
Publisher
Springer Science and Business Media LLC
Online
2019-06-14
DOI
10.1038/s41467-019-10689-w
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Note: Only part of the references are listed.- Comprehensive behavioral analysis of the Cdkl5 knockout mice revealed significant enhancement in anxiety- and fear-related behaviors and impairment in both acquisition and long-term retention of spatial reference memory
- (2018) Kosuke Okuda et al. PLoS One
- Mice lacking cyclin-dependent kinase-like 5 manifest autistic and ADHD-like behaviors
- (2017) Cian-Ling Jhang et al. HUMAN MOLECULAR GENETICS
- Loss of CDKL5 in Glutamatergic Neurons Disrupts Hippocampal Microcircuitry and Leads to Memory Impairment in Mice
- (2017) Sheng Tang et al. JOURNAL OF NEUROSCIENCE
- Biotin tagging of MeCP2 in mice reveals contextual insights into the Rett syndrome transcriptome
- (2017) Brian S Johnson et al. NATURE MEDICINE
- CDKL5 controls postsynaptic localization of GluN2B-containing NMDA receptors in the hippocampus and regulates seizure susceptibility
- (2017) Kosuke Okuda et al. NEUROBIOLOGY OF DISEASE
- Dendritic Spine Instability in a Mouse Model of CDKL5 Disorder Is Rescued by Insulin-like Growth Factor 1
- (2016) Grazia Della Sala et al. BIOLOGICAL PSYCHIATRY
- Least-Squares Means: TheRPackagelsmeans
- (2016) Russell V. Lenth Journal of Statistical Software
- Synaptic Synthesis, Dephosphorylation, and Degradation
- (2015) Paolo La Montanara et al. JOURNAL OF BIOLOGICAL CHEMISTRY
- Fitting Linear Mixed-Effects Models Usinglme4
- (2015) Douglas Bates et al. Journal of Statistical Software
- Social deficits in IRSp53 mutant mice improved by NMDAR and mGluR5 suppression
- (2015) Woosuk Chung et al. NATURE NEUROSCIENCE
- From the genetic architecture to synaptic plasticity in autism spectrum disorder
- (2015) Thomas Bourgeron NATURE REVIEWS NEUROSCIENCE
- Excitatory/Inhibitory Balance and Circuit Homeostasis in Autism Spectrum Disorders
- (2015) Sacha B. Nelson et al. NEURON
- Cell types in the mouse cortex and hippocampus revealed by single-cell RNA-seq
- (2015) A. Zeisel et al. SCIENCE
- Suppression of NMDA receptor function in mice prenatally exposed to valproic acid improves social deficits and repetitive behaviors
- (2015) Jaeseung Kang et al. Frontiers in Molecular Neuroscience
- Autism-Associated Neuroligin-3 Mutations Commonly Impair Striatal Circuits to Boost Repetitive Behaviors
- (2014) Patrick E. Rothwell et al. CELL
- Mapping Pathological Phenotypes in a Mouse Model of CDKL5 Disorder
- (2014) Elena Amendola et al. PLoS One
- Preparation of Synaptic Plasma Membrane and Postsynaptic Density Proteins Using a Discontinuous Sucrose Gradient
- (2014) Marie Kristel Bermejo et al. Jove-Journal of Visualized Experiments
- Evaluation of Voltage-Sensitive Fluorescence Dyes for Monitoring Neuronal Activity in the Embryonic Central Nervous System
- (2013) Saad Habib-E-Rasul Mullah et al. JOURNAL OF MEMBRANE BIOLOGY
- Memantine Rescues Transient Cognitive Impairment Caused by High-Molecular-Weight A Oligomers But Not the Persistent Impairment Induced by Low-Molecular-Weight Oligomers
- (2013) C. P. Figueiredo et al. JOURNAL OF NEUROSCIENCE
- Mechanisms of epileptogenesis: a convergence on neural circuit dysfunction
- (2013) Ethan M. Goldberg et al. NATURE REVIEWS NEUROSCIENCE
- Palmitoylation-dependent CDKL5-PSD-95 interaction regulates synaptic targeting of CDKL5 and dendritic spine development
- (2013) Y.-C. Zhu et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- Development of home cage social behaviors in BALB/cJ vs. C57BL/6J mice
- (2012) Andrew H. Fairless et al. BEHAVIOURAL BRAIN RESEARCH
- Autistic-like behaviour in Scn1a +/− mice and rescue by enhanced GABA-mediated neurotransmission
- (2012) Sung Han et al. NATURE
- CDKL5 ensures excitatory synapse stability by reinforcing NGL-1–PSD95 interaction in the postsynaptic compartment and is impaired in patient iPSC-derived neurons
- (2012) Sara Ricciardi et al. NATURE CELL BIOLOGY
- Down syndrome: the brain in trisomic mode
- (2012) Mara Dierssen NATURE REVIEWS NEUROSCIENCE
- Loss of CDKL5 disrupts kinome profile and event-related potentials leading to autistic-like phenotypes in mice
- (2012) I.-T. J. Wang et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- Network hyperexcitability in hippocampal slices from Mecp2 mutant mice revealed by voltage-sensitive dye imaging
- (2011) Gaston Calfa et al. JOURNAL OF NEUROPHYSIOLOGY
- Hippocampal microcircuit dynamics probed using optical imaging approaches
- (2011) Douglas A. Coulter et al. JOURNAL OF PHYSIOLOGY-LONDON
- Neocortical excitation/inhibition balance in information processing and social dysfunction
- (2011) Ofer Yizhar et al. NATURE
- CDKL5, a Protein Associated with Rett Syndrome, Regulates Neuronal Morphogenesis via Rac1 Signaling
- (2010) Q. Chen et al. JOURNAL OF NEUROSCIENCE
- Dysfunction in GABA signalling mediates autism-like stereotypies and Rett syndrome phenotypes
- (2010) Hsiao-Tuan Chao et al. NATURE
- CDKL5 Expression Is Modulated during Neuronal Development and Its Subcellular Distribution Is Tightly Regulated by the C-terminal Tail
- (2008) Laura Rusconi et al. JOURNAL OF BIOLOGICAL CHEMISTRY
- GABA Regulates Excitatory Synapse Formation in the Neocortex via NMDA Receptor Activation
- (2008) D. D. Wang et al. JOURNAL OF NEUROSCIENCE
- In vitro functional imaging in brain slices using fast voltage-sensitive dye imaging combined with whole-cell patch recording
- (2008) Greg C Carlson et al. Nature Protocols
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