DOCSLIB.ORG

T€ Brain-Derived Neurotrophic Factor Overexpression Induces Precocious Critical Period in Mouse Visual Cortex

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
T€ Brain-Derived Neurotrophic Factor Overexpression Induces Precocious Critical Period in Mouse Visual Cortex The Journal of Neuroscience, 1999, Vol. 19 RC40 1of5 Brain-derived Neurotrophic Factor Overexpression Induces Precocious Critical Period in Mouse Visual Cortex Jessica L. Hanover,1 Z. Josh Huang,2 Susumu Tonegawa,2,3 and Michael P. Stryker1 1Neuroscience Graduate Program and Department of Physiology, University of California, San Francisco, California, 94143, and 2Howard Hughes Medical Institute, Center for Learning and Memory, Center for Cancer Research and Department of Biology, and 3Department of Brain and Cognitive Science, Massachusetts Institute of Technology, Cambridge, Massachusetts, 02139 Brain-derived neurotrophic factor (BDNF) is a candidate mole- found that unlike the infusion experiments, excess BDNF ex- cule for regulating activity-dependent synaptic plasticity on the pressed in mouse visual cortex did not block ocular dominance grounds of its expression pattern in developing visual cortex plasticity. Instead, single neurons in V1 of the BDNF transgenic and that of its receptor, trkB (Castre´ n et al., 1992; Bozzi et al., mice were as susceptible to the effects of monocular depriva- 1995; Schoups et al., 1995; Cabelli et al., 1996), as well as the tion (MD) as neurons in wild-type mice, but only during a modulation of these patterns by activity (Castre´ n et al., 1992; precocious critical period. At a time when V1 in the wild-type Bozzi et al., 1995; Schoups et al., 1995). Infusing trkB ligands or mouse responded maximally toa4dMDwith a reduction in its their neutralizing agents, the trkB-IgG fusion proteins, into vi- response to deprived eye visual stimulation, the transgenic sual cortex alters the development and plasticity of ocular mouse V1 had already passed the peak of its precocious critical dominance columns (Cabelli et al., 1995; Riddle et al., 1995; period and no longer responded maximally. This finding sug- Galuske et al., 1996; Gillespie et al., 1996; Cabelli et al., 1997). gests a role for BDNF in promoting the postnatal maturation of To test further the physiological role of BDNF, we studied a cortical circuitry. transgenic mouse that expresses elevated levels of BDNF in Key words: BDNF; visual cortex; critical period; neurotrophin; primary visual cortex (V1) postnatally (Huang et al., 1999). We trkB; ocular dominance; plasticity; transgenic mouse Several experiments implicate brain-derived neurotrophic factor known to affect inhibitory circuitry in cortical neurons (Ruther- (BDNF) in models of neuronal plasticity in vitro, including the ford et al., 1997). enhancement of cortical cell dendritic morphology (McAllister et The role of neurotrophins in the development and plasticity of al., 1995), the enhancement of synaptic transmission (Kang and rodent visual cortex is well established. Exogenous nerve growth Schuman, 1995; Carmignoto et al., 1997; Rutherford et al., 1998), factor (NGF) in rats can block ocular dominance plasticity or and the induction and maintenance of long-term potentiation in substitute for visual experience, and antibodies to NGF block hippocampus (Korte et al., 1995; Figurov et al., 1996; Patterson et normal development of cortical visual responses despite normal al., 1996). Results from experiments in vivo are also consistent visual experience (Maffei et al., 1992; Berardi et al., 1994; Fagio- with the idea that competition for limiting quantities of BDNF or lini and Stryker, 1996; Fagiolini et al., 1997). In most earlier other endogenous trkB ligands regulates synaptic plasticity during experiments, exogenous BDNF has been applied pharmacologi- development of visual cortex by acting as the “reward” for the cally in high concentration. In transgenic mice in which a BDNF more active inputs that are more successful in driving the transgene was linked to the calcium/calmodulin-dependent ki- postsynaptic partners. In carnivores, providing excess trkB ligand nase II a (aCaMKII) promoter, the levels of BDNF in cortex blocks the further segregation of geniculocortical inputs into were only moderately elevated in the cells that normally express nascent ocular dominance columns and, perhaps by rewarding BDNF (Huang et al., 1999). Abnormalities in such animals could deprived and nondeprived inputs indiscriminately, prevents the illuminate the physiological roles played by BDNF in visual usual loss of responsiveness of cortical neurons to the deprived cortical development. eye after monocular deprivation (MD) (Cabelli et al., 1995, 1996; As in wild-type animals, neocortical levels of BDNF in BDNF- Galuske et al., 1996; Gillespie et al., 1996). Blocking endogenous trkB ligands also alters cortical development (Cabelli et al., 1997). In addition to its effects on excitatory neurons, BDNF is also This article is published in The Journal of Neuroscience, Rapid Communications Section, which publishes brief, peer- reviewed papers online, not in print. Rapid Communications Received Aug. 10, 1999; revised Sept. 15, 1999; accepted Sept. 20, 1999. are posted online approximately one month earlier than they This work was supported by National Institutes of Health Grants NS16033 (M.P.S.) and NS32925 (S.T.), the Damon Runyon–Walter Winchell Foundation (to would appear if printed. They are listed in the Table of Z.J.H.) and a National Eye Institute vision training grant (J.L.H.). We thank A. Contents of the next open issue of JNeurosci. Cite this article Antonini, N. Priebe, and M. Silver for helpful discussions. as: JNeurosci, 1999, 19:RC40 (1–5). The publication date is Correspondence should be addressed to Prof. Michael P. Stryker, Department of Physiology, Room S-762, 513 Parnassus Avenue, University of California, San the date of posting online at www.jneurosci.org. Francisco, CA 94143-0444. E-mail: [email protected]. Copyright © 1999 Society for Neuroscience 0270-6474/99/190001-05$05.00/0 http://www.jneurosci.org/cgi/content/full/3687 2of5 J. Neurosci., 1999, Vol. 19 Hanover et al. • Critical Period for Cortex in BDNF Overexpresser overexpressing transgenic mice increased during postnatal devel- opment. BDNF mRNA expression in the cerebral cortex of the transgenic mice was accelerated by postnatal day 2 (P2), at which time the wild-type littermates showed very low levels of endoge- nous BDNF. By 3 weeks of age, total BDNF mRNA levels in the transgenic neocortex were significantly higher than those in wild- type animals of 5 weeks of age. At 5 weeks, BDNF mRNA levels in transgenic mouse neocortex were three times normal, and in adult transgenic mice, they were five times normal (Huang et al., 1999). MATERIALS AND METHODS Generation of mutant mice. Mice were generated as described previously (Huang et al., 1999). In the present study, experiments were performed on the A9 line of mice. In these animals, the expression pattern of the transgene was mainly restricted to forebrain, including the neocortex and hippocampus. Within the cortex, the expression of the transgene had the laminar pattern of the endogenous genes for BDNF or aCaMKII. In the visual cortex of both transgenic and wild-type animals, highest levels of BDNF expression were in layers II/III and V/VI; however, in transgenic animals, BDNF expression levels were substantially higher in all cortical layers. These higher levels of BDNF expression resulted from increase in the number of neurons expressing BDNF as well as an increase in the intensity of BDNF immunoreactivity in the neurons. In addition, the transgene appeared not to be expressed by neurons with inhibitory markers (Huang et al., 1999). Monocular deprivation. Lid sutures were performed as described (Gor- don and Stryker, 1996), except that anesthesia was produced using 2.5% isoflurane (Abbott, North Chicago, IL) in oxygen. Animals were checked daily to make sure that the sutured eye remained closed. If any sutures appeared loose, they were replaced under anesthesia. In the cases in which holes were apparent and the eye could have been exposed, the animals were removed from the study. Electrophysiology. Mice were prepared blind to genotype under Nem- butal (50 mg/kg; Abbott) and chlorprothixene (0.2 mg; Sigma, St. Louis, MO) anesthesia using standard protocol (Gordon and Stryker, 1996). In each animal, single cells separated by at least 50 mm were recorded from multiple penetration sites within the V1 binocular zone (BZ) contralat- eral to the deprived eye using extracellular tungsten microelectrodes. All recordings were contralateral to the deprived eye. Receptive fields were plotted on a tangent screen with a hand-held projection lamp or computer-generated stimuli. Only cells with receptive fields within the central 25° of the visual hemifield were included in this study. The cells were assigned to an ocular dominance group according to the classifica- tion scheme of Hubel and Wiesel (1962). Cells were assigned to group 1 if they responded only to stimuli presented to the contralateral (de- prived) eye and 7 if they responded only to stimuli presented to the ipsilateral (nondeprived) eye. Cells responding equally well to stimuli presented to each eye individually were assigned to group 4, and groups 2 or 3 and 5 or 6 indicated cells responding better to stimuli presented to the contralateral and ipsilateral eyes, respectively. Ocular dominance histograms such as in Figure 2a–h show percent of cells as a function of Figure 1. Visually evoked response properties of neurons in Tg and WT ocular dominance group. The contralateral bias index (CBI) was then adult mouse V1. a, Raster plot of single-unit responses from a neuron in calculated, a weighted average of the bias for one eye or the other, with the Tg mouse V1 BZ in response to computer-generated, moving, ori- 5 2 1 2 1 2 the following formula: CBI [(n1 n7) (2/3)(n2 n6) (1/3)(n3 ented light bars (0–315°) as well as to no stimulus [spontaneous (Spont)]. 1 5 5 n5) N]/2N, where n total number of cells, and nx number of cells Stimuli consisted of three repetitions at each of eight orientations. Spikes with ocular dominance scores equal to x. Each neuron was also assigned were continuously recorded before, during, and after the stimulus moved a habituation score on a scale of 0 to 3; a score of 0 indicated a neuron through the receptive field (indicated with an oval) of the neuron.
Load more

Recommended publications
  • A Critical Period for Second Language Acquisition: Evidence from 2/3 Million English Speakers ⁎ Joshua K
    Cognition xxx (xxxx) xxx–xxx Contents lists available at ScienceDirect Cognition journal homepage: www.elsevier.com/locate/cognit Original Articles A critical period for second language acquisition: Evidence from 2/3 million English speakers ⁎ Joshua K. Hartshornea,b, , Joshua B. Tenenbauma, Steven Pinkerc a Department of Brain & Cognitive Sciences, Massachusetts Institute of Technology, Building 46, 77 Massachusetts Avenue, MIT, Cambridge, MA 02139, United States b Department of Psychology, Boston College, McGuinn Hall 527, Chestnut Hill, MA 02467, United States c Department of Psychology, Harvard University, William James Hall 970, 33 Kirkland St., Cambridge, MA 02138, United States ARTICLE INFO ABSTRACT Keywords: Children learn language more easily than adults, though when and why this ability declines have been obscure Language acquisition for both empirical reasons (underpowered studies) and conceptual reasons (measuring the ultimate attainment Critical period of learners who started at different ages cannot by itself reveal changes in underlying learning ability). We L2 acquisition address both limitations with a dataset of unprecedented size (669,498 native and non-native English speakers) and a computational model that estimates the trajectory of underlying learning ability by disentangling current age, age at first exposure, and years of experience. This allows us to provide the first direct estimate of how grammar-learning ability changes with age, finding that it is preserved almost to the crux of adulthood (17.4 years old) and then declines steadily. This finding held not only for “difficult” syntactic phenomena but also for “easy” syntactic phenomena that are normally mastered early in acquisition. The results support the existence of a sharply-defined critical period for language acquisition, but the age of offset is much later than previously speculated.
    [Show full text]
  • The Evolution of the Critical Period for Language Acquisition:'
    Cognifion. 40( 1991) 159-201 The evolution of the critical period for language acquisition:’ Received March 14. 1990. final revision accepted May 15, 1991 Abstract Hurford. J.R.. IYYI. The evolution of the critical period for language acqukition. Cognition. 10: 159-201. E\.idence suggests that there is a critical, or at least a setuiti1.e. period for language acquisition, which ends around puberty. The existence of this perioti is explained by an evolutionary model which assumes that (a) linguistic ability is in principle (if not in practice) measurable, and (b) the amount of language controlled by at1 individual conferred selective advantage on it. In this model. the language fault? is seen as adaptive, favoured by natural selection. bthile tfle critical period for language acquisition itself is not an adaptation, but arises from the interplay of genetic factors influencing life-history characters in relation to language acqnisitiotl. The evolutionary model is implemented on a computer and simulations of popula- tions evolving under various plausible. if idealized, conditions result in clear critical period effects, which end around puberty. 1. The phenomenon to he explained A body of evidence suggests that there is in humans a critical period, or at least a sensitive period, for the acquisition of (first) language. The critical period hypothesis was most prominently advanced by Lenneberg (1967), a work which *I thank the following for helpful discussion or comments on this paper: Jean Aitchison. Ellen Bard. James Cooke Brown. Phil Carr. Peter Caryl, Grev Corbett. Tim Ingold, Steve Isard. Aubrey Manning, David Smillie, John Maynard Smith, Jim Monaghan.
    [Show full text]
  • Role of Perineuronal Nets in Neural Plasticity
    The Journal of Neuroscience, November 9, 2016 • 36(45):11459–11468 • 11459 Mini-Symposium Casting a Wide Net: Role of Perineuronal Nets in Neural Plasticity Barbara A. Sorg,1 XSabina Berretta,2 XJordan M. Blacktop,1 XJames W. Fawcett,3 XHiroshi Kitagawa,4 X Jessica C.F. Kwok,5 and XMarta Miquel6 1Department of Integrative Physiology and Neuroscience, Translational Addiction Research Center, Washington State University, Vancouver, Washington 98686, 2Translational Neuroscience Laboratory, McLean Hospital, Mailman Research Center, Belmont, Massachusetts 02478, 3John van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge CB2 0SP, United Kingdom, 4Department of Biochemistry, Kobe Pharmaceutical, University, Kobe 658-8558, Japan, 5School of Biomedical Sciences, University of Leeds, Leeds LS2 9JT, United Kingdom, and 6Faculty of Health Sciences, Psychobiology, Universitat Jaume I, 12071 Castello´n de la Plana, Spain Perineuronal nets (PNNs) are unique extracellular matrix structures that wrap around certain neurons in the CNS during development and control plasticity in the adult CNS. They appear to contribute to a wide range of diseases/disorders of the brain, are involved in recovery from spinal cord injury, and are altered during aging, learning and memory, and after exposure to drugs of abuse. Here the focus isonhowamajorcomponentofPNNs,chondroitinsulfateproteoglycans,controlplasticity,andontheroleofPNNsinmemoryinnormal aging, in a tauopathy model of Alzheimer’s disease, and in drug addiction. Also discussed is how altered extracellular matrix/PNN formation during development may produce synaptic pathology associated with schizophrenia, bipolar disorder, major depression, and autism spectrum disorders. Understanding the molecular underpinnings of how PNNs are altered in normal physiology and disease will offer insights into new treatment approaches for these diseases.
    [Show full text]
  • An Extracellular Perspective on CNS Maturation: Perineuronal Nets and the Control of Plasticity
    International Journal of Molecular Sciences Review An Extracellular Perspective on CNS Maturation: Perineuronal Nets and the Control of Plasticity Daniela Carulli 1,2,* and Joost Verhaagen 1 1 Laboratory for Neuroregeneration, Netherlands Institute for Neuroscience, Royal Academy of Arts and Sciences, 1105 BA Amsterdam, The Netherlands; [email protected] 2 Department of Neuroscience Rita Levi-Montalcini and Neuroscience Institute Cavalieri Ottolenghi, University of Turin, 10040 Turin, Italy * Correspondence: [email protected] Abstract: During restricted time windows of postnatal life, called critical periods, neural circuits are highly plastic and are shaped by environmental stimuli. In several mammalian brain areas, from the cerebral cortex to the hippocampus and amygdala, the closure of the critical period is dependent on the formation of perineuronal nets. Perineuronal nets are a condensed form of an extracellular matrix, which surrounds the soma and proximal dendrites of subsets of neurons, enwrapping synaptic terminals. Experimentally disrupting perineuronal nets in adult animals induces the reactivation of critical period plasticity, pointing to a role of the perineuronal net as a molecular brake on plasticity as the critical period closes. Interestingly, in the adult brain, the expression of perineuronal nets is remarkably dynamic, changing its plasticity-associated conditions, including memory processes. In this review, we aimed to address how perineuronal nets contribute to the maturation of brain circuits and the regulation of adult brain plasticity and memory processes in physiological and pathological conditions. Citation: Carulli, D.; Verhaagen, J. An Extracellular Perspective on CNS Keywords: perineuronal net; critical period; chondroitin sulfate proteoglycans; learning; memory; Maturation: Perineuronal Nets and Alzheimer’s disease; drug addiction the Control of Plasticity.
    [Show full text]
  • What's Critical for the Minireview Critical Period in Visual Cortex?
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Cell, Vol. 99, 673±676, December 23, 1999, Copyright 1999 by Cell Press What's Critical for the Minireview Critical Period in Visual Cortex? Lawrence C. Katz adults had virtually no effect. Subsequent anatomical Howard Hughes Medical Institute and tracing revealed that the imbalance of activity resulted Department of Neurobiology in the actual loss of synaptic inputs from the thalamic Duke University Medical Center regions representing the closed eye, and expansion of Durham, North Carolina 27710 those representing the open eye (Figure 1B). While in normal primates and cats, the thalamic inputs represent- ing the two eyes parse cortical layer 4 into alternating, During a brief period in postnatal life, sensory experi- equal-sized stripes, eye closure during the critical period ences indelibly shape the behavior of many vertebrate reduced the cortical territory of the closed eye to species. Salmon learn their natal rivers, birds learn their shrunken broken stripes, with its former territory now father's songs, and humans acquire language based invaded by inputs representing the other eye (Hubel et on particular sensory experiences during such ªcritical al., 1977). Behaviorally, animals monocularly deprived periods.º Early ethological investigations of critical peri- ods focused on the behavioral consequences of early sensory experiences, but how and where such experi- ences were permanently etched into brain circuits was unknown. The notion that critical periods actually repre- sented heightened epochs of brain plasticity, and that ex- perience could produce permanent, large-scale changes in neuronal circuits emerged from Hubel and Wiesel's investigations in the cat and monkey visual cortex begin- ning in the mid-1960s (Hubel and Wiesel, 1970).
    [Show full text]
  • Critical & Sensitive Periods
    Critical & Sensitive Periods Concept History Methods Critical Period: The Concept A critical period is a time during an organism’s life span when it is more sensitive to environmental influences or stimulation than at other times during its life. Critical Period: The Semantics • Critical period: – begins and ends abruptly – period beyond which a phenomenon will not appear • Sensitive period: – begins and ends gradually – period of maximal sensitivity • Window of opportunity: – popular metaphor – introduced by P. Bateson, 1978 in his critique Critical Period: Embryology As is well known, a certain organ arises much earlier or later in the embryo than certain others. When the primary developmental changes are on the verge of taking place or when an important organ is entering its initial stage of rapid proliferation or budding, a serious interruption of the developmental progress often causes decided injuries to this particular organ, while only slight or no ill effects may be suffered by the embryo in general. Such particular sensitive periods during development I have termed ‘critical moments.’ -- Charles R. Stockard Am. J. of Anat. 1921 28:115-275, p. 139 Critical Period: Induction Embryonic cells transplanted before (but not after) a certain stage of development are induced, by influences in their new cellular environment to develop like cells typical of the new site, not as they would have developed at their original site. -- Hans Spemann, 1938 Critical Period: The Frogs No Eye Rotation 180° Eye Rotation 180° Eye Rotation 24 Hours Later
    [Show full text]
  • Targeting Oxidative Stress and Aberrant Critical Period Plasticity in the Developmental Trajectory to Schizophrenia
    Schizophrenia Bulletin vol. 41 no. 4 pp. 835–846, 2015 doi:10.1093/schbul/sbv065 Advance Access publication June 1, 2015 Targeting Oxidative Stress and Aberrant Critical Period Plasticity in the Developmental Trajectory to Schizophrenia Kim Q. Do1, Michel Cuenod1, and Takao K. Hensch*,2 1 Center for Psychiatric Neuroscience, Department of Psychiatry, Lausanne University Hospital-CHUV, Prilly-Lausanne, Switzerland; Downloaded from 2Center for Brain Science, Department of Molecular Cellular Biology, Harvard University, Cambridge, MA *To whom correspondence should be addressed; Center for Brain Science, Department of Molecular Cellular Biology, Harvard University, 52 Oxford Street, Cambridge, MA 02138, US; tel: +1-617-384-5882; fax: +1-617-495-4038; e-mail: [email protected] http://schizophreniabulletin.oxfordjournals.org/ Schizophrenia is a neurodevelopmental disorder reflect- In healthy development, convergent multisensory ing a convergence of genetic risk and early life stress. inputs are progressively selected in order to filter the The slow progression to first psychotic episode represents salient ones and focus attention. This process is funda- both a window of vulnerability as well as opportunity mental to establish “common sense” knowledge and “nat- for therapeutic intervention. Here, we consider recent ural self-evidence” notions (eg, “the sky is blue and above neurobiological insight into the cellular and molecular the earth” or “young people will become old”) which components of developmental critical periods and their are typically settled and confirmed during development. vulnerability to redox dysregulation. In particular, the Their deficits lead to basic symptoms2 and disorders of consistent loss of parvalbumin-positive interneuron the self believed to be central to the phenomenology of (PVI) function and their surrounding perineuronal nets schizophrenia (SZ; see reviews by Parnas3,4).
    [Show full text]
  • Brain Mechanisms Underlying the Critical Period for Language: Linking Theory and Practice
    Brain Mechanisms Underlying the Critical Period for Language: Linking Theory and Practic e Patricia K. Kuhl Introduction Half a century ago, humans’ capacity for speech and language provoked classic debates on what it means to be human by strong proponents of na - tivism (Chomsky, 1959) and learning (Skinner, 1957). The debate centered on learning and development, and the remarkable transition that all children make as they acquire a language. While we are now far beyond these debates and informed by a great deal of data about infants, their innate predisposi - tions and incredible abilities to learn once exposed to natural language (Kuhl, 2009; Saffran, Werker, and Werner, 2006), we are still just breaking ground with regard to the neural mechanisms that underlie language de - velopment and its ‘critical period’ (see Friederici and Wartenburger, 2010; Kuhl and Rivera-Gaxiola, 2008; Kuhl et al ., 2008). Developmental neuro - science is beginning to deepen our understanding of the nature of language and its ‘window of opportunity’ for learning. To explore the topic of the critical period for language, and its practical implications, I will focus on the youngest learners – infants in the first year of life – and compare them to adult learners. The linguistic data will focus on the most elementary units of language – the consonants and vowels that make up words. Infants’ responses to the basic building blocks of speech provide an experimentally accessible window on the roles of nature and nurture in language acquisition. Comparative studies at the phonetic level have allowed us to examine humans’ unique language processing abilities at birth and as they respond to language experience.
    [Show full text]
  • Forever Young: Neoteny, Neurogenesis and a Critique of Critical Periods in Olfaction David M. Coppola & Leonard E. White
    Forever young: Neoteny, neurogenesis and a critique of critical periods in olfaction David M. Coppola & Leonard E. White Journal of Bioenergetics and Biomembranes ISSN 0145-479X J Bioenerg Biomembr DOI 10.1007/s10863-018-9778-4 1 23 Your article is protected by copyright and all rights are held exclusively by Springer Science+Business Media, LLC, part of Springer Nature. This e-offprint is for personal use only and shall not be self-archived in electronic repositories. If you wish to self- archive your article, please use the accepted manuscript version for posting on your own website. You may further deposit the accepted manuscript version in any repository, provided it is only made publicly available 12 months after official publication or later and provided acknowledgement is given to the original source of publication and a link is inserted to the published article on Springer's website. The link must be accompanied by the following text: "The final publication is available at link.springer.com”. 1 23 Author's personal copy Journal of Bioenergetics and Biomembranes https://doi.org/10.1007/s10863-018-9778-4 MINI-REVIEW Forever young: Neoteny, neurogenesis and a critique of critical periods in olfaction David M. Coppola1 & Leonard E. White2 Received: 2 September 2018 /Accepted: 1 November 2018 # Springer Science+Business Media, LLC, part of Springer Nature 2018 Abstract The critical period concept has been one of the most transcendent in science, education, and society forming the basis of our fixation on ‘quality’ of childhood experiences. The neural basis of this process has been revealed in developmental studies of visual, auditory and somatosensory maps and their enduring modification through manipulations of experience early in life.
    [Show full text]
  • A Critical Period That Shapes Motor Circuits
    News & views mode to transverse vibrations. This previously e-mails: [email protected]; Phys. Rev. Lett. 119, 057604 (2017). unseen vortex motion indicates that an [email protected] 5. Luk’yanchuk, I., Sené, A. & Vinokur, V. M. Phys. Rev. B 98, 024107 (2018). instability accompanies a structural transi- 1. Li, Q. et al. Nature 592, 376–380 (2021). 6. Landau, L. D. & Lifshitz, E. M. Phys. Z. Sowjet. 8, 153–169 tion to a state in which the vortex centres form 2. Zhang, Q., Herchig, R. & Ponomareva, I. Phys. Rev. Lett. (1935). a zigzag chain. Compared with the 0.08-THz 107, 177601 (2011). 7. Kittel, C. Phys. Rev. 70, 965–971 (1946). 3. Gui, Z. & Bellaiche, L. Phys. Rev. B 89, 064303 8. De Guerville, F., Luk’yanchuk, I., Lahoche, L. & mode, those at 0.3–0.4 THz are associated (2014). El Marssi, M. Mater. Sci. Eng. B 120, 16–20 (2005). with more-intricate vortex dynamics and can 4. Hlinka, J., Paściak, M., Körbel, S. & Marton, P. 9. Yadav, A. K. et al. Nature 530, 198–201 (2016). be less easily attributed to a particular type of vibration. Neuroscience To unravel the full picture of vortex dynamics, future work needs to distinguish between inter-vortex motion, intra-vortex motion and vortex bending. Moreover, the A critical period that longitudinal mode of vibration must be iden- tified. This mode is associated with a sequence shapes motor circuits of alternating displacements of domain walls (the boundaries between domains) and has Laura Sancho & Nicola J. Allen remarkable properties that arise from the associated dynamics of surface charges.
    [Show full text]
  • Sensitive Periods in the Development of the Brain and Behavior
    Sensitive Periods in the Development of the Brain and Behavior Eric I. Knudsen Abstract & Experience exerts a profound influence on the brain and, tecture of a circuit in fundamental ways, causing certain pat- therefore, on behavior. When the effect of experience on the terns of connectivity to become highly stable and, therefore, brain is particularly strong during a limited period in energetically preferred. Plasticity that occurs beyond the end development, this period is referred to as a sensitive period. of a sensitive period, which is substantial in many circuits, Such periods allow experience to instruct neural circuits to alters connectivity patterns within the architectural constraints process or represent information in a way that is adaptive for established during the sensitive period. Preferences in a cir- the individual. When experience provides information that is cuit that result from experience during sensitive periods are essential for normal development and alters performance illustrated graphically as changes in a ‘‘stability landscape,’’ a permanently, such sensitive periods are referred to as critical metaphor that represents the relative contributions of genetic periods. and experiential influences in shaping the information pro- Although sensitive periods are reflected in behavior, they cessing capabilities of a neural circuit. By understanding sen- are actually a property of neural circuits. Mechanisms of plas- sitive periods at the circuit level, as well as understanding the ticity at the circuit level are discussed that have been shown relationship between circuit properties and behavior, we gain to operate during sensitive periods. A hypothesis is proposed a deeper insight into the critical role that experience plays in that experience during a sensitive period modifies the archi- shaping the development of the brain and behavior.
    [Show full text]
  • UNIVERSITY of CALIFORNIA Los Angeles a Transient Microcircuit Underlying Critical Period Plasticity in the Visual Cortex a Disse
    UNIVERSITY OF CALIFORNIA Los Angeles A transient microcircuit underlying critical period plasticity in the visual cortex A dissertation submitted in partial satisfaction of the requirements for the degree of Doctor of Philosophy in Neuroscience by Courtney Yaeger 2018 © Copyright by Courtney Yaeger 2018 iii ABSTRACT OF THE DISSERTATION A transient microcircuit underlying critical period plasticity in the visual cortex by Courtney Yaeger Doctor of Philosophy in Neuroscience University of California, Los Angeles, 2018 Professor Joshua Trachtenberg, Chair During so-called critical periods of early postnatal life, sensory experience profoundly and permanently sculpts cortical neural circuitry. After critical period closure, experience- dependent plasticity is dramatically limited, and it is not known what differentiates juvenile and adult plasticity mechanisms. At its core, plasticity is a dendritic phenomenon, and in the cortex, plasticity is determined by changes in sensory input and cortical state. Here we show that dendritic and somatic activity in pyramidal neurons is fundamentally different across critical period closure due to the cholinergic engagement of inhibitory circuitry. At the peak of the critical period, acetylcholine released from the basal forebrain directly excites somatostatin-expressing (SST) interneurons. The resultant inhibition of pyramidal cell dendrites and of fast-spiking, parvalbumin-expressing (PV) inhibitory neurons enhances branch-specific dendritic responses and increases somatic spiking within pyramidal neurons.
    [Show full text]