Tau reduction affects excitatory and inhibitory neurons differently, reduces excitation/inhibition ratios, and counteracts network hypersynchrony

[1]  L. Mucke,et al.  Tau: Enabler of diverse brain disorders and target of rapidly evolving therapeutic strategies , 2021, Science.

[2]  Brian R. Lee,et al.  Integrated Morphoelectric and Transcriptomic Classification of Cortical GABAergic Cells , 2020, Cell.

[3]  K. Kullander,et al.  A prefrontal–paraventricular thalamus circuit requires juvenile social experience to regulate adult sociability in mice , 2020, Nature Neuroscience.

[4]  Alice D. Lam,et al.  Association of epileptiform abnormalities and seizures in Alzheimer disease , 2020, Neurology.

[5]  P. Kind,et al.  Input-Output Relationship of CA1 Pyramidal Neurons Reveals Intact Homeostatic Mechanisms in a Mouse Model of Fragile X Syndrome , 2020, Cell reports.

[6]  A. Boxer,et al.  Targeting tau: Clinical trials and novel therapeutic approaches , 2020, Neuroscience Letters.

[7]  Ming-Rong Zhang,et al.  Selective Disruption of Inhibitory Synapses Leading to Neuronal Hyperexcitability at an Early Stage of Tau Pathogenesis in a Mouse Model , 2020, The Journal of Neuroscience.

[8]  L. Bouwman,et al.  Perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA) acutely affect human α1β2γ2L GABAA receptor and spontaneous neuronal network function in vitro , 2020, Scientific Reports.

[9]  L. Mucke,et al.  Tau Reduction Prevents Key Features of Autism in Mouse Models , 2020, Neuron.

[10]  Guilherme Neves,et al.  Activity-Dependent Plasticity of Axo-axonic Synapses at the Axon Initial Segment , 2020, Neuron.

[11]  Jian-Zhi Wang,et al.  Interneuron Accumulation of Phosphorylated tau Impairs Adult Hippocampal Neurogenesis by Suppressing GABAergic Transmission. , 2020, Cell stem cell.

[12]  Shiaoching Gong,et al.  Pathogenic Tau Impairs Axon Initial Segment Plasticity and Excitability Homeostasis , 2019, Neuron.

[13]  D. Schubert,et al.  Neuronal network dysfunction in a human model for Kleefstra syndrome mediated by enhanced NMDAR signaling , 2019, bioRxiv.

[14]  A. Konnerth,et al.  A vicious cycle of β amyloid–dependent neuronal hyperactivation , 2019, Science.

[15]  Brian R. Lee,et al.  Classification of electrophysiological and morphological neuron types in the mouse visual cortex , 2019, Nature Neuroscience.

[16]  J. Rubenstein,et al.  Excitation-inhibition balance as a framework for investigating mechanisms in neuropsychiatric disorders , 2019, Molecular Psychiatry.

[17]  J. Krystal,et al.  Altered Connectivity in Depression: GABA and Glutamate Neurotransmitter Deficits and Reversal by Novel Treatments , 2019, Neuron.

[18]  I. Nelken,et al.  Tau impairs neural circuits, dominating amyloid-β effects, in Alzheimer models in vivo , 2018, Nature Neuroscience.

[19]  Evan Z. Macosko,et al.  Molecular Diversity and Specializations among the Cells of the Adult Mouse Brain , 2018, Cell.

[20]  Takashi Kawashima,et al.  A genetically encoded fluorescent sensor for in vivo imaging of GABA , 2018, Nature Methods.

[21]  Samuel Frere,et al.  Alzheimer’s Disease: From Firing Instability to Homeostasis Network Collapse , 2018, Neuron.

[22]  J. Pancrazio,et al.  Spontaneous and Evoked Activity from Murine Ventral Horn Cultures on Microelectrode Arrays , 2017, Front. Cell. Neurosci..

[23]  T. Fath,et al.  Tau exacerbates excitotoxic brain damage in an animal model of stroke , 2017, Nature Communications.

[24]  Timothy A. Miller,et al.  Tau reduction prevents neuronal loss and reverses pathological tau deposition and seeding in mice with tauopathy , 2017, Science Translational Medicine.

[25]  D. Xia,et al.  Hyperphosphorylated tau causes reduced hippocampal CA1 excitability by relocating the axon initial segment , 2017, Acta Neuropathologica.

[26]  T. Südhof,et al.  Modulation of excitation on parvalbumin interneurons by neuroligin-3 regulates the hippocampal network , 2016, Nature Neuroscience.

[27]  Heidi E Kirsch,et al.  Incidence and impact of subclinical epileptiform activity in Alzheimer's disease , 2016, Annals of neurology.

[28]  L. Mucke,et al.  Network abnormalities and interneuron dysfunction in Alzheimer disease , 2016, Nature Reviews Neuroscience.

[29]  Hillel Adesnik,et al.  Inhibitory Circuits in Cortical Layer 5 , 2016, Front. Neural Circuits.

[30]  C. Hoogenraad,et al.  Cooperative Interactions between 480 kDa Ankyrin-G and EB Proteins Assemble the Axon Initial Segment , 2016, The Journal of Neuroscience.

[31]  S. Maeda,et al.  Expression of A152T human tau causes age‐dependent neuronal dysfunction and loss in transgenic mice , 2016, EMBO reports.

[32]  A. Kanner Management of psychiatric and neurological comorbidities in epilepsy , 2016, Nature Reviews Neurology.

[33]  E. Chang,et al.  Purification and Characterization of Progenitor and Mature Human Astrocytes Reveals Transcriptional and Functional Differences with Mouse , 2016, Neuron.

[34]  M. Evans,et al.  Rapid Modulation of Axon Initial Segment Length Influences Repetitive Spike Firing , 2015, Cell reports.

[35]  J. Nurnberger,et al.  Differential responses to lithium in hyperexcitable neurons from patients with bipolar disorder , 2015, Nature.

[36]  G. Schellenberg,et al.  High copy wildtype human 1N4R tau expression promotes early pathological tauopathy accompanied by cognitive deficits without progressive neurofibrillary degeneration , 2015, Acta neuropathologica communications.

[37]  E. Stern,et al.  Pathological Tau Disrupts Ongoing Network Activity , 2015, Neuron.

[38]  K. Staley Molecular mechanisms of epilepsy , 2015, Nature Neuroscience.

[39]  T. Maniatis,et al.  An RNA-Sequencing Transcriptome and Splicing Database of Glia, Neurons, and Vascular Cells of the Cerebral Cortex , 2014, The Journal of Neuroscience.

[40]  L. Mucke,et al.  Tau Reduction Prevents Disease in a Mouse Model of Dravet Syndrome , 2014, Annals of neurology.

[41]  William A. Catterall,et al.  Impaired excitability of somatostatin- and parvalbumin-expressing cortical interneurons in a mouse model of Dravet syndrome , 2014, Proceedings of the National Academy of Sciences.

[42]  Alois Schlögl,et al.  Stimfit: quantifying electrophysiological data with Python , 2013, Front. Neuroinform..

[43]  J. Serratosa,et al.  Hyperexcitability and epileptic seizures in a model of frontotemporal dementia , 2013, Neurobiology of Disease.

[44]  Ethan M. Goldberg,et al.  Mechanisms of epileptogenesis: a convergence on neural circuit dysfunction , 2013, Nature Reviews Neuroscience.

[45]  M. Evans,et al.  Calcineurin Signaling Mediates Activity-Dependent Relocation of the Axon Initial Segment , 2013, The Journal of Neuroscience.

[46]  S. Younkin,et al.  Tau Loss Attenuates Neuronal Network Hyperexcitability in Mouse and Drosophila Genetic Models of Epilepsy , 2013, The Journal of Neuroscience.

[47]  J. Luebke,et al.  Electrophysiological changes precede morphological changes to frontal cortical pyramidal neurons in the rTg4510 mouse model of progressive tauopathy , 2012, Acta Neuropathologica.

[48]  Keith A. Vossel,et al.  Levetiracetam suppresses neuronal network dysfunction and reverses synaptic and cognitive deficits in an Alzheimer’s disease model , 2012, Proceedings of the National Academy of Sciences.

[49]  Laurence O Trussell,et al.  The physiology of the axon initial segment. , 2012, Annual review of neuroscience.

[50]  Edward O. Mann,et al.  Inhibitory Interneuron Deficit Links Altered Network Activity and Cognitive Dysfunction in Alzheimer Model , 2012, Cell.

[51]  Yousheng Shu,et al.  Short- and Long-Term Plasticity at the Axon Initial Segment , 2011, The Journal of Neuroscience.

[52]  H. Vacher,et al.  End-binding proteins EB3 and EB1 link microtubules to ankyrin G in the axon initial segment , 2011, Proceedings of the National Academy of Sciences.

[53]  L. Mucke,et al.  Amyloid-β/Fyn–Induced Synaptic, Network, and Cognitive Impairments Depend on Tau Levels in Multiple Mouse Models of Alzheimer's Disease , 2011, The Journal of Neuroscience.

[54]  M. Cuccaro,et al.  Autism and epilepsy: Historical perspective , 2010, Brain and Development.

[55]  Jürgen Götz,et al.  Dendritic Function of Tau Mediates Amyloid-β Toxicity in Alzheimer's Disease Mouse Models , 2010, Cell.

[56]  M. Grubb,et al.  Activity-dependent relocation of the axon initial segment fine-tunes neuronal excitability , 2010, Nature.

[57]  Harunori Ohmori,et al.  Presynaptic activity regulates Na+ channel distribution at the axon initial segment , 2010, Nature.

[58]  F. Jensen,et al.  Epileptogenesis in the immature brain: emerging mechanisms , 2009, Nature Reviews Neurology.

[59]  Xiaoli Li,et al.  Synchronization measurement of multiple neuronal populations. , 2007, Journal of neurophysiology.

[60]  S. Charpier,et al.  Deep Layer Somatosensory Cortical Neurons Initiate Spike-and-Wave Discharges in a Genetic Model of Absence Seizures , 2007, The Journal of Neuroscience.

[61]  L. Mucke,et al.  Reducing Endogenous Tau Ameliorates Amyloid ß-Induced Deficits in an Alzheimer's Disease Mouse Model , 2007, Science.

[62]  M. Goedert,et al.  Ordered Assembly of Tau Protein and Neurodegeneration. , 2019, Advances in experimental medicine and biology.

[63]  J. Ávila,et al.  Tau regulates the localization and function of End‐binding proteins 1 and 3 in developing neuronal cells , 2015, Journal of neurochemistry.

[64]  David F. Meaney,et al.  Dynamic Changes in Neural Circuit Topology Following Mild Mechanical Injury In Vitro , 2011, Annals of Biomedical Engineering.