The Experts below are selected from a list of 306 Experts worldwide ranked by ideXlab platform

Takao K. Hensch - One of the best experts on this subject based on the ideXlab platform.

  • single nucleus rna sequencing of mouse auditory cortex reveals Critical Period triggers and brakes
    Proceedings of the National Academy of Sciences of the United States of America, 2020
    Co-Authors: Takao K. Hensch, Tania Rinaldi Barkat, Brian T Kalish, Erin E Diel, Elizabeth J Zhang, Michael E Greenberg
    Abstract:

    Auditory experience drives neural circuit refinement during windows of heightened brain plasticity, but little is known about the genetic regulation of this developmental process. The primary auditory cortex (A1) of mice exhibits a Critical Period for thalamocortical connectivity between postnatal days P12 and P15, during which tone exposure alters the tonotopic topography of A1. We hypothesized that a coordinated, multicellular transcriptional program governs this window for patterning of the auditory cortex. To generate a robust multicellular map of gene expression, we performed droplet-based, single-nucleus RNA sequencing (snRNA-seq) of A1 across three developmental time points (P10, P15, and P20) spanning the tonotopic Critical Period. We also tone-reared mice (7 kHz pips) during the 3-d Critical Period and collected A1 at P15 and P20. We identified and profiled both neuronal (glutamatergic and GABAergic) and nonneuronal (oligodendrocytes, microglia, astrocytes, and endothelial) cell types. By comparing normal- and tone-reared mice, we found hundreds of genes across cell types showing altered expression as a result of sensory manipulation during the Critical Period. Functional voltage-sensitive dye imaging confirmed GABA circuit function determines Critical Period onset, while Nogo receptor signaling is required for its closure. We further uncovered previously unknown effects of developmental tone exposure on trajectories of gene expression in interneurons, as well as candidate genes that might execute tonotopic plasticity. Our single-nucleus transcriptomic resource of developing auditory cortex is thus a powerful discovery platform with which to identify mediators of tonotopic plasticity.

  • inhibitory circuit gating of auditory Critical Period plasticity
    Nature Neuroscience, 2018
    Co-Authors: Takao K. Hensch, Anne E Takesian, Luke J Bogart, Jeff W Lichtman
    Abstract:

    Cortical sensory maps are remodeled during early life to adapt to the surrounding environment. Both sensory and contextual signals are important for induction of this plasticity, but how these signals converge to sculpt developing thalamocortical circuits remains largely unknown. Here we show that layer 1 (L1) of primary auditory cortex (A1) is a key hub where neuromodulatory and topographically organized thalamic inputs meet to tune the cortical layers below. Inhibitory interneurons in L1 send narrowly descending projections to differentially modulate thalamic drive to pyramidal and parvalbumin-expressing (PV) cells in L4, creating brief windows of intracolumnar activation. Silencing of L1 (but not VIP-expressing) cells abolishes map plasticity during the tonotopic Critical Period. Developmental transitions in nicotinic acetylcholine receptor (nAChR) sensitivity in these cells caused by Lynx1 protein can be overridden to extend Critical-Period closure. Notably, thalamocortical maps in L1 are themselves stable, and serve as a scaffold for cortical plasticity throughout life.

  • Valproate reopens Critical-Period learning of absolute pitch
    Frontiers in systems neuroscience, 2013
    Co-Authors: Judit Gervain, Takao K. Hensch, Bradley W. Vines, Lawrence M. Chen, Rubo J. Seo, Janet F. Werker, Allan H. Young
    Abstract:

    Absolute pitch, the ability to identify or produce the pitch of a sound without a reference point, has a Critical Period, i.e. it can only be acquired early in life. However, research has shown that histone-deacetylase inhibitors (HDAC inhibitors) enable adult mice to establish perceptual preferences that are otherwise impossible to acquire after youth. In humans, we found that adult men who took valproate (a HDAC inhibitor) learned to identify pitch significantly better than those taking placebo – evidence that valproate facilitated Critical-Period learning in the adult human brain. Importantly, this result was not due to a general change in cognitive function, but rather a specific effect on a sensory task associated with a Critical-Period.

  • Critical Period for acoustic preference in mice
    Proceedings of the National Academy of Sciences, 2012
    Co-Authors: Eun-jin Yang, Eric Lin, Takao K. Hensch
    Abstract:

    Preference behaviors are often established during early life, but the underlying neural circuit mechanisms remain unknown. Adapting a unique nesting behavior assay, we confirmed a “Critical Period” for developing music preference in C57BL/6 mice. Early music exposure between postnatal days 15 and 24 reversed their innate bias for silent shelter, which typically could not be altered in adulthood. Instead, exposing adult mice treated acutely with valproic acid or carrying a targeted deletion of the Nogo receptor (NgR−/−) unmasked a strong plasticity of preference consistent with a reopening of the Critical Period as seen in other systems. Imaging of cFos expression revealed a prominent neuronal activation in response to the exposed music in the prelimbic and infralimbic medial prefrontal cortex only under conditions of open plasticity. Neither behavioral changes nor selective medial prefrontal cortex activation was observed in response to pure tone exposure, indicating a music-specific effect. Open-field center crossings were increased concomitant with shifts in music preference, suggesting a potential anxiolytic effect. Thus, music may offer both a unique window into the emotional state of mice and a potentially efficient assay for molecular “brakes” on Critical Period plasticity common to sensory and higher order brain areas.

  • A Critical Period for auditory thalamocortical connectivity
    Nature neuroscience, 2011
    Co-Authors: Tania Rinaldi Barkat, Daniel B. Polley, Takao K. Hensch
    Abstract:

    The authors isolated the refinement of auditory thalamocortical connectivity by in vivo recordings and day-by-day voltage-sensitive dye imaging in an acute brain slice preparation. They find that postnatal connectivity between thalamus and cortex determines a Critical Period for plasticity in the auditory system. Neural circuits are shaped by experience during Periods of heightened brain plasticity in early postnatal life. Exposure to acoustic features produces age-dependent changes through largely unresolved cellular mechanisms and sites of origin. We isolated the refinement of auditory thalamocortical connectivity by in vivo recordings and day-by-day voltage-sensitive dye imaging in an acute brain slice preparation. Passive tone-rearing modified response strength and topography in mouse primary auditory cortex (A1) during a brief, 3-d window, but did not alter tonotopic maps in the thalamus. Gene-targeted deletion of a forebrain-specific cell-adhesion molecule (Icam5) accelerated plasticity in this Critical Period. Consistent with its normal role of slowing spinogenesis, loss of Icam5 induced precocious stubby spine maturation on pyramidal cell dendrites in neocortical layer 4 (L4), identifying a primary locus of change for the tonotopic plasticity. The evolving postnatal connectivity between thalamus and cortex in the days following hearing onset may therefore determine a Critical Period for auditory processing.

Mark Hübener - One of the best experts on this subject based on the ideXlab platform.

  • Critical-Period Plasticity in the Visual Cortex
    Annual Review of Neuroscience, 2012
    Co-Authors: Christiaan N. Levelt, Mark Hübener
    Abstract:

    In many regions of the developing brain, neuronal circuits undergo defined phases of enhanced plasticity, termed Critical Periods. Work in the rodent visual cortex has led to important insights into the cellular and molecular mechanisms regulating the timing of the Critical Period. Although there is little doubt that the maturation of specific inhibitory circuits plays a key role in the opening of the Critical Period in the visual cortex, it is less clear what puts an end to it. In this review, we describe the established mechanisms and point out where more experimental work is needed. We also show that plasticity in the visual cortex is present well before, and long after, the peak of the Critical Period.

Joshua T. Trachtenberg - One of the best experts on this subject based on the ideXlab platform.

  • Neuromodulatory control of localized dendritic spiking in Critical Period cortex.
    Nature, 2019
    Co-Authors: Courtney E. Yaeger, Dario L. Ringach, Joshua T. Trachtenberg
    Abstract:

    Sensory experience in early postnatal life, during so-called Critical Periods, restructures neural circuitry to enhance information processing1. Why the cortex is susceptible to sensory instruction in early life and why this susceptibility wanes with age are unclear. Here we define a developmentally restricted engagement of inhibitory circuitry that shapes localized dendritic activity and is needed for vision to drive the emergence of binocular visual responses in the mouse primary visual cortex. We find that at the peak of the Critical Period for binocular plasticity, acetylcholine released from the basal forebrain during Periods of heightened arousal directly excites somatostatin (SST)-expressing interneurons. Their inhibition of pyramidal cell dendrites and of fast-spiking, parvalbumin-expressing interneurons enhances branch-specific dendritic responses and somatic spike rates within pyramidal cells. By adulthood, this cholinergic sensitivity is lost, and compartmentalized dendritic responses are absent but can be re-instated by optogenetic activation of SST cells. Conversely, suppressing SST cell activity during the Critical Period prevents the normal development of binocular receptive fields by impairing the maturation of ipsilateral eye inputs. This transient cholinergic modulation of SST cells, therefore, seems to orchestrate two features of neural plasticity—somatic disinhibition and compartmentalized dendritic spiking. Loss of this modulation may contribute to Critical Period closure. A transient circuit that links cholinergic neuromodulation and inhibition is responsible for the dendritic compartmentalization of evoked responses in the mouse visual cortex during the Critical Period of robust plasticity.

  • neuromodulatory control of localized dendritic spiking in Critical Period cortex
    Nature, 2019
    Co-Authors: Courtney E. Yaeger, Dario L. Ringach, Joshua T. Trachtenberg
    Abstract:

    Sensory experience in early postnatal life, during so-called Critical Periods, restructures neural circuitry to enhance information processing1. Why the cortex is susceptible to sensory instruction in early life and why this susceptibility wanes with age are unclear. Here we define a developmentally restricted engagement of inhibitory circuitry that shapes localized dendritic activity and is needed for vision to drive the emergence of binocular visual responses in the mouse primary visual cortex. We find that at the peak of the Critical Period for binocular plasticity, acetylcholine released from the basal forebrain during Periods of heightened arousal directly excites somatostatin (SST)-expressing interneurons. Their inhibition of pyramidal cell dendrites and of fast-spiking, parvalbumin-expressing interneurons enhances branch-specific dendritic responses and somatic spike rates within pyramidal cells. By adulthood, this cholinergic sensitivity is lost, and compartmentalized dendritic responses are absent but can be re-instated by optogenetic activation of SST cells. Conversely, suppressing SST cell activity during the Critical Period prevents the normal development of binocular receptive fields by impairing the maturation of ipsilateral eye inputs. This transient cholinergic modulation of SST cells, therefore, seems to orchestrate two features of neural plasticity-somatic disinhibition and compartmentalized dendritic spiking. Loss of this modulation may contribute to Critical Period closure.

Xiaojie Huang - One of the best experts on this subject based on the ideXlab platform.

  • Silent synapse: A new player in visual cortex Critical Period plasticity.
    Pharmacological research, 2019
    Co-Authors: Xiaojie Huang
    Abstract:

    Abstract During Critical Period, the heightened plasticity in neocortex opens a time window when, with proper external environmental stimuli, experience dependent refinement processes help to optimize the function of neuronal networks. With the closure of Critical Periods, the gradually decreased plasticity leaves a mature system which is stable to perform its function but with limited plasticity for changes in the adult. In order to gain more detailed knowledge about Critical Period plasticity, ocular dominance plasticity in primary visual cortex has been used as a study model to test plasticity levels in neural circuits. Since then, multiple cellular and molecular mechanisms have been proposed. Among them, the abundance of AMPA receptor silent synapses, as substrates for Hebbian plasticity, is shown to be closely related to not only Critical Period plasticity, but also the network refinement at glutamatergic synapses of principal neurons. Here, I discuss the role of silent synapses and how they interact with other known mechanisms involved in Critical Period plasticity.

Kathleen R. Zahs - One of the best experts on this subject based on the ideXlab platform.

  • Critical Period control in sensory cortex
    Current opinion in neurobiology, 1994
    Co-Authors: Kevin Fox, Kathleen R. Zahs
    Abstract:

    The search continues for factors whose regulation during development accounts for the end of the Critical Period for experience-dependent cortical plasticity. Recent studies suggest that NMDA receptors and neurotrophins may be involved either individually or in concert. NMDA receptor subunits are developmentally regulated in a way that affects the kinetic properties of the NMDA receptor. The expression of mRNAs for neurotrophins and their receptors is regulated by developmental factors and by neuronal activity, and exogenous neurotrophins block Critical Period plasticity in the visual cortex.