A5100335376- Neuroscience and Neuropharmacology Research
- Neural dynamics and brain function
- Autism Spectrum Disorder Research
- Photoreceptor and optogenetics research
- Genetics and Neurodevelopmental Disorders
- Receptor Mechanisms and Signaling
- Neuroinflammation and Neurodegeneration Mechanisms
- Pluripotent Stem Cells Research
- CRISPR and Genetic Engineering
- Neurogenesis and neuroplasticity mechanisms
- Ion channel regulation and function
- Congenital heart defects research
- Neurobiology and Insect Physiology Research
- Neuroscience and Neural Engineering
- Epilepsy research and treatment
- Biochemical Analysis and Sensing Techniques
- Neurotransmitter Receptor Influence on Behavior
- ATP Synthase and ATPases Research
- Child Nutrition and Feeding Issues
- Mitochondrial Function and Pathology
- Visual perception and processing mechanisms
- Marine animal studies overview
- RNA Research and Splicing
- Tryptophan and brain disorders
- Hearing, Cochlea, Tinnitus, Genetics
Washington University in St. Louis
2019-2025
Peking University Shenzhen Hospital
2025
Shenzhen Bay Laboratory
2020-2024
Peking University
2010-2023
Harvard University
2021-2023
Boston Children's Hospital
2021-2023
Beijing Academy of Artificial Intelligence
2020
Tsinghua University
2020
Beijing University of Chinese Medicine
2019
Howard Hughes Medical Institute
2015-2018
Abstract Background Dravet syndrome is a devastating infantile-onset epilepsy with cognitive deficits and autistic traits caused by genetic alterations in SCN1A gene encoding the α-subunit of voltage-gated sodium channel Na v 1.1. Disease modeling using patient-derived induced pluripotent stem cells (iPSCs) can be powerful tool to reproduce this syndrome’s human pathology. However, no such effort has been reported date. We here report cellular model for DS that utilizes iPSCs. Results...
Neuroligins are evolutionarily conserved postsynaptic cell adhesion molecules that interact with presynaptic neurexins. Neurons express multiple neuroligin isoforms targeted to specific synapses, but their synaptic functions and mechanistic redundancy not completely understood. Overexpression or RNAi-mediated knockdown of neuroligins, respectively, causes a dramatic increase decrease in synapse density, whereas genetic deletions neuroligins impair function only minor effects on numbers,...
Abstract Proteins critical for synaptic transmission are non-uniformly distributed and assembled into regions of high density called subsynaptic densities (SSDs) that transsynaptically align in nanocolumns. Neurexin-1 neurexin-3 essential presynaptic adhesion molecules non-redundantly control NMDAR- AMPAR-mediated transmission, respectively, via transsynaptic interactions with distinct postsynaptic ligands. Despite their functional relevance, fundamental questions regarding the nanoscale...
The subsynaptic organization of postsynaptic neurotransmitter receptors into nanoclusters that are aligned with presynaptic release sites is essential for the high fidelity synaptic transmission. However, mechanisms controlling nanoscale in vivo remain incompletely understood. Here, we deconstructed role neuroligin-3 (Nlgn3), a adhesion molecule linked to autism, organizing AMPA-type glutamate calyx Held synapse. Deletion
Glutamate-induced excitotoxicity has been implicated in the etiology of stroke, epilepsy, and neurodegenerative diseases. NMDA receptors (NMDARs) play a pivotal role excitotoxic injury; however, clinical trials testing NMDAR antagonists as neuroprotectants have discouraging. The development novel neuroprotectant molecules is being vigorously pursued. Here, we report that downstream regulatory element antagonist modulator (DREAM) significantly inhibits surface expression NMDARs NMDAR-mediated...
<title>Abstract</title> Cell adhesion molecules (CAMs) are pivotal in establishing and maintaining synaptic connectivity. Emerging evidence indicates that some secreted factors within the cleft, including C1q-like proteins (C1qls), play a crucial role bridging pre- post-synapses by connecting bilateral CAMs. However, mechanisms of those synapse assembly remain incomplete. Here, we explored C1ql-mediated connectivity, focusing on C1ql1 its post-synaptic receptor brain-specific angiogenesis...
Abstract Neuroligin-3 ( Nlgn3 ) is an autism-associated cell-adhesion molecule that interacts with neurexins and robustly expressed in both neurons astrocytes. Neuronal essential regulator of synaptic transmission but the function astrocytic largely unknown. Given high penetrance mutations autism emerging role astrocytes neuropsychiatric disorders, we here asked whether might shape neural circuit properties cerebellum similar to neuronal . Imaging tagged protein produced by...
In human patients, loss-of-function mutations of the postsynaptic cell-adhesion molecule neuroligin-4 were repeatedly identified as monogenetic causes autism. mice, deletions caused autism-related behavioral impairments and subtle changes in synaptic transmission, was found, at least part, glycinergic synapses. However, low expression levels precluded a comprehensive analysis localization, overexpression puzzlingly impaired excitatory but not inhibitory function. As result, function remains...
Expanded polyglutamine (polyQ) tract in the human TATA-box-binding protein (hTBP) causes neurodegenerative disease spinocerebellar ataxia 17 (SCA17). To investigate pathological effects of polyQ expansion, we established a SCA17 model Drosophila . Similar to patients, transgenic flies expressing mutant hTBP with an expanded (hTBP80Q) exhibit progressive neurodegeneration, late-onset locomotor impairment and shortened lifespan. Microarray analysis reveals that hTBP80Q widespread...
Abstract Background Autism spectrum disorder (ASD) is a neurodevelopmental with pronounced heritability in the general population. This largely attributable to effects of polygenic susceptibility, inherited liability exhibiting distinct sex differences phenotypic expression. Attempts model ASD human cellular systems have principally involved rare de novo mutations associated phenocopies. However, by definition, these models are not representative liability, which accounts for vast share...
Age-related hearing loss (AHL) is the most common sensory disorder in elderly population. Dysfunction of spiral ganglion neurons (SGNs) a major contributor to AHL. Previously, we showed that one changes aging auditory system SGN excitability increase mice (i.e., AHL mice) compared with young ones, which raised possibility SGNs may contribute Since hyperpolarization-activated cyclic nucleotide-gated (HCN) channels play important roles determining neuronal excitability, predicted HCN are...
Abstract Background Phelan-McDermid Syndrome (PMS) is a rare condition caused by deletion or mutation of the SHANK3 gene. Individuals with PMS frequently present intellectual disability, autism spectrum disorder, and other neurodevelopmental challenges. Electroencephalography (EEG) can provide window into network-level function in PMS. Methods Here, we analyze EEG data collected across multiple sites individuals (n = 26) typically developing 15). We quantify oscillatory power, alpha-gamma...
Non‐technical summary Information is coded in the form of bursts electrical impulses propagating among nerve cells which complex networks brain. Effective communication between these depends on ability for cross‐talk them through release and reception chemical substances (neurotransmitters). This study uses hearing system as a model to show that patterns can dramatically impact amount neurotransmitter released. When presented short clusters, are more effective releasing neurotransmitters...