A5003220448- Neuroscience and Neuropharmacology Research
- Neural dynamics and brain function
- Photoreceptor and optogenetics research
- Retinal Development and Disorders
- Genetics and Neurodevelopmental Disorders
- Birth, Development, and Health
- Visual perception and processing mechanisms
- Memory and Neural Mechanisms
- Neuroendocrine regulation and behavior
- Neurogenesis and neuroplasticity mechanisms
- Proteoglycans and glycosaminoglycans research
- Epilepsy research and treatment
- Ion channel regulation and function
- Single-cell and spatial transcriptomics
- Anesthesia and Neurotoxicity Research
- Sleep and Wakefulness Research
- Neuroinflammation and Neurodegeneration Mechanisms
- Neurobiology and Insect Physiology Research
- Anesthesia and Sedative Agents
- Olfactory and Sensory Function Studies
- Adolescent and Pediatric Healthcare
- Diet and metabolism studies
- Ophthalmology and Visual Impairment Studies
- Autism Spectrum Disorder Research
- Circadian rhythm and melatonin
Boston Children's Hospital
2016-2025
Harvard University
2016-2025
The University of Tokyo
1991-2025
Boston University
2021-2024
National Institute of Mental Health
2019-2023
Center for Pain and the Brain
2016-2022
Queensland Centre for Mental Health Research
2022
RIKEN Center for Brain Science
2007-2021
Canadian Institute for Advanced Research
2014-2020
Imaging Center
2013-2020
This study describes comprehensive polling of transcription start and termination sites analysis previously unidentified full-length complementary DNAs derived from the mouse genome. We identify 5' 3' boundaries 181,047 transcripts with extensive variation in arising alternative promoter usage, splicing, polyadenylation. There are 16,247 new protein-coding transcripts, including 5154 encoding proteins. Genomic mapping transcriptome reveals transcriptional forests, overlapping on both...
Sensory experience in early life shapes the mammalian brain. An impairment activity-dependent refinement of functional connections within developing visual cortex was identified here a mouse model. Gene-targeted disruption one isoform glutamic acid decarboxylase prevented competitive loss responsiveness to an eye briefly deprived vision, without affecting cooperative mechanisms synapse modification vitro. Selective, use-dependent enhancement fast intracortical inhibitory transmission with...
Loss-of-function mutations in human SCN1A gene encoding Nav1.1 are associated with a severe epileptic disorder known as myoclonic epilepsy infancy. Here, we generated and characterized knock-in mouse line loss-of-function nonsense mutation the Scn1a gene. Both homozygous heterozygous mice developed seizures within first postnatal month. Immunohistochemical analyses revealed that, developing neocortex, was clustered predominantly at axon initial segments of parvalbumin-positive (PV)...
Abstract One unifying explanation for the complexity of Autism Spectrum Disorders (ASD) may lie in disruption excitatory/inhibitory (E/I) circuit balance during critical periods development. We examined whether Parvalbumin (PV)-positive inhibitory neurons, which normally drive experience-dependent refinement (Hensch Nat Rev Neurosci 6:877–888, 1), are disrupted across heterogeneous ASD mouse models. performed a meta-analysis PV expression previously published models and analyzed two...
Weak inhibition within visual cortex early in life prevents experience-dependent plasticity. Loss of responsiveness to an eye deprived vision can be initiated prematurely by enhancing γ-aminobutyric acid (GABA)–mediated transmission with benzodiazepines. Here, we use a mouse “knockin” mutation α subunits that renders individual GABA type A (GABA ) receptors insensitive diazepam show particular inhibitory network controls expression the critical period. Only α1-containing circuits were found...
A hallmark of schizophrenia pathophysiology is the dysfunction cortical inhibitory GABA neurons expressing parvalbumin, which are essential for coordinating neuronal synchrony during various sensory and cognitive tasks. The high metabolic requirements these fast-spiking cells may render them susceptible to redox dysregulation oxidative stress. Using mice carrying a genetic imbalance, we demonstrate that extracellular perineuronal nets, constitute specialized polyanionic matrix enwrapping...
Specific transfer of (orthodenticle homeobox 2) Otx2 homeoprotein into GABAergic interneurons expressing parvalbumin (PV) is necessary and sufficient to open, then close, a critical period (CP) plasticity in the developing mouse visual cortex. The accumulation endogenous PV cells suggests presence specific binding sites. Here, we find that perineuronal nets (PNNs) on surfaces permit specific, constitutive capture Otx2. We identify 15 aa domain containing an arginine-lysine doublet (RK...
Experience-dependent brain plasticity typically declines after an early critical period during which circuits are established. Loss of with closure the limits improvement function in adulthood, but mechanisms that change brain's remain poorly understood. Here, we identified increase expression Lynx1 protein mice prevented primary visual cortex late life. Removal this molecular brake enhanced nicotinic acetylcholine receptor signaling. thus maintains stability mature cortical networks...
Parvalbumin inhibitory interneurons (PVIs) are crucial for maintaining proper excitatory/inhibitory balance and high-frequency neuronal synchronization. Their activity supports critical developmental trajectories, sensory cognitive processing, social behavior. Despite heterogeneity in the etiology across schizophrenia autism spectrum disorder, PVI circuits altered these psychiatric disorders. Identifying mechanism(s) underlying deficits is essential to establish treatments targeting...