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Pesquisa : F02.463.425.209 [Categoria DeCS]
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  1 / 890 MEDLINE  
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PMID:29287884
Autor:Kim BJ; Kim J; Park IY; Jung JY; Suh MW; Oh SH
Endereço:Wide River Institute of Immunology, Seoul National University College of Medicine, Seoul, South Korea.
Título:Effects of transient auditory deprivation during critical periods on the development of auditory temporal processing.
Fonte:Int J Pediatr Otorhinolaryngol; 104:66-71, 2018 Jan.
ISSN:1872-8464
País de publicação:Ireland
Idioma:eng
Resumo:OBJECTIVES: The central auditory pathway matures through sensory experiences and it is known that sensory experiences during periods called critical periods exert an important influence on brain development. The present study aimed to investigate whether temporary auditory deprivation during critical periods (CPs) could have a detrimental effect on the development of auditory temporal processing. MATERIALS AND METHODS: Twelve neonatal rats were randomly assigned to control and study groups; Study group experienced temporary (18-20 days) auditory deprivation during CPs (Early deprivation study group). Outcome measures included changes in auditory brainstem response (ABR), gap prepulse inhibition of the acoustic startle reflex (GPIAS), and gap detection threshold (GDT). To further delineate the specific role of CPs in the outcome measures above, the same paradigm was applied in adult rats (Late deprivation group) and the findings were compared with those of the neonatal rats. RESULTS: Soon after the restoration of hearing, early deprivation study animals showed a significantly lower GPIAS at intermediate gap durations and a larger GDT than early deprivation controls, but these differences became insignificant after subsequent auditory inputs. Additionally, the ABR results showed significantly delayed latencies of waves IV, V, and interpeak latencies of wave I-III and wave I-V in study group. Late deprivation group didn't exhibit any deterioration in temporal processing following sensory deprivation. CONCLUSION: Taken together, the present results suggest that transient auditory deprivation during CPs might cause reversible disruptions in the development of temporal processing.
Tipo de publicação: JOURNAL ARTICLE


  2 / 890 MEDLINE  
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PMID:29184199
Autor:Sommeijer JP; Ahmadlou M; Saiepour MH; Seignette K; Min R; Heimel JA; Levelt CN
Endereço:Department of Molecular Visual Plasticity, Netherlands Institute for Neuroscience, Royal Netherlands Academy of Arts and Sciences, Amsterdam, The Netherlands.
Título:Thalamic inhibition regulates critical-period plasticity in visual cortex and thalamus.
Fonte:Nat Neurosci; 20(12):1715-1721, 2017 Dec.
ISSN:1546-1726
País de publicação:United States
Idioma:eng
Resumo:During critical periods of development, experience shapes cortical circuits, resulting in the acquisition of functions used throughout life. The classic example of critical-period plasticity is ocular dominance (OD) plasticity, which optimizes binocular vision but can reduce the responsiveness of the primary visual cortex (V1) to an eye providing low-grade visual input. The onset of the critical period of OD plasticity involves the maturation of inhibitory synapses within V1, specifically those containing the GABA receptor α1 subunit. Here we show that thalamic relay neurons in mouse dorsolateral geniculate nucleus (dLGN) also undergo OD plasticity. This process depends on thalamic α1-containing synapses and is required for consolidation of the OD shift in V1 during long-term deprivation. Our findings demonstrate that thalamic inhibitory circuits play a central role in the regulation of the critical period. This has far-reaching consequences for the interpretation of studies investigating the molecular and cellular mechanisms regulating critical periods of brain development.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Gabra1 protein, mouse); 0 (Receptors, GABA-A)


  3 / 890 MEDLINE  
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PMID:28628196
Autor:Begum MR; Sng JCG
Endereço:Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Título:Molecular mechanisms of experience-dependent maturation in cortical GABAergic inhibition.
Fonte:J Neurochem; 142(5):649-661, 2017 Sep.
ISSN:1471-4159
País de publicação:England
Idioma:eng
Resumo:Critical periods (CP) in early post-natal life are periods of plasticity during which the neuronal circuitry is most receptive to environmental stimuli. These early experiences translate to a more permanent and sophisticated neuronal connection in the adult brain systems. Multiple studies have pointed to the development of inhibitory circuitry as one of the central factors for the onset of critical periods. We discuss several molecular mechanisms regulating inhibitory circuit maturation and CP, from gene transcription level to protein signaling level. Also, beyond the level of gene sequences, we briefly consider recent information on dynamic epigenetic regulation of gene expression through histone methylation and acetylation and their implication on timed development of the inhibitory circuitry for the onset of CP.
Tipo de publicação: JOURNAL ARTICLE; REVIEW
Nome de substância:56-12-2 (gamma-Aminobutyric Acid)


  4 / 890 MEDLINE  
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PMID:28615475
Autor:Alberini CM; Travaglia A
Endereço:Center for Neural Science, New York University, New York, New York 10003 ca60@nyu.edu.
Título:Infantile Amnesia: A Critical Period of Learning to Learn and Remember.
Fonte:J Neurosci; 37(24):5783-5795, 2017 Jun 14.
ISSN:1529-2401
País de publicação:United States
Idioma:eng
Resumo:Infantile amnesia, the inability of adults to recollect early episodic memories, is associated with the rapid forgetting that occurs in childhood. It has been suggested that infantile amnesia is due to the underdevelopment of the infant brain, which would preclude memory consolidation, or to deficits in memory retrieval. Although early memories are inaccessible to adults, early-life events, such as neglect or aversive experiences, can greatly impact adult behavior and may predispose individuals to various psychopathologies. It remains unclear how a brain that rapidly forgets, or is not yet able to form long-term memories, can exert such a long-lasting and important influence. Here, with a particular focus on the hippocampal memory system, we review the literature and discuss new evidence obtained in rats that illuminates the paradox of infantile amnesia. We propose that infantile amnesia reflects a developmental critical period during which the learning system is learning how to learn and remember.
Tipo de publicação: JOURNAL ARTICLE; REVIEW


  5 / 890 MEDLINE  
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PMID:28500220
Autor:Levine JN; Chen H; Gu Y; Cang J
Endereço:Department of Neurobiology.
Título:Environmental Enrichment Rescues Binocular Matching of Orientation Preference in the Mouse Visual Cortex.
Fonte:J Neurosci; 37(24):5822-5833, 2017 Jun 14.
ISSN:1529-2401
País de publicação:United States
Idioma:eng
Resumo:Neural circuits are shaped by experience during critical periods of development. Sensory deprivation during these periods permanently compromises an organism's ability to perceive the outside world. In the mouse visual system, normal visual experience during a critical period in early life drives the matching of individual cortical neurons' orientation preferences through the two eyes, likely a key step in the development of binocular vision. Here, in mice of both sexes, we show that the binocular matching process is completely blocked by monocular deprivation spanning the entire critical period. We then show that 3 weeks of environmental enrichment (EE), a paradigm of enhanced sensory, motor, and cognitive stimulation, is sufficient to rescue binocular matching to the level seen in unmanipulated mice. In contrast, 6 weeks of conventional housing only resulted in a partial rescue. Finally, we use two-photon calcium imaging to track the matching process chronically in individual cells during EE-induced rescue. We find that for cells that are clearly dominated by one of the two eyes, the input representing the weaker eye changes its orientation preference to align with that of the dominant eye. These results thus reveal ocular dominance as a key driver of the binocular matching process, and suggest a model whereby the dominant input instructs the development of the weaker input. Such a mechanism may operate in the development of other systems that need to integrate inputs from multiple sources to generate normal neuronal functions. Critical periods are developmental windows of opportunity that ensure the proper wiring of neural circuits, as well as windows of vulnerability when abnormal experience could cause lasting damage to the developing brain. In the visual system, critical period plasticity drives the establishment of binocularly matched orientation preferences in cortical neurons. Here, we show that binocular matching is completely blocked by monocular deprivation during the critical period. Moreover, environmental enrichment can fully rescue the disrupted matching, whereas conventional housing of twice the duration results in a partial rescue. We then use two-photon calcium imaging to track individual cells chronically during the EE-induced recovery, and reveal important insights into how appropriate function can be restored to the nervous system after the critical period.
Tipo de publicação: JOURNAL ARTICLE


  6 / 890 MEDLINE  
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PMID:28114886
Autor:Izumi H; Ishimoto T; Yamamoto H; Mori H
Endereço:Department of Molecular Neuroscience, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Toyama, 930-0194, Japan.
Título:Application of hairless mouse strain to bioluminescence imaging of Arc expression in mouse brain.
Fonte:BMC Neurosci; 18(1):18, 2017 Jan 23.
ISSN:1471-2202
País de publicação:England
Idioma:eng
Resumo:BACKGROUND: Bioluminescence imaging (BLI) is a powerful technique for monitoring the temporal and spatial dynamics of gene expression in the mouse brain. However, the black fur, skin pigmentation and hair regrowth after depilation of mouse interfere with BLI during developmental and daily examination. The aim of this study was to extend the application of Arc-Luc transgenic (Tg) mice to the BLI of neuronal activity in the mouse brain by introducing the hairless (HL) gene and to examine Arc-Luc expression at various developmental stages without interference from black fur, skin pigmentation, and hair regrowth. RESULTS: The Arc-Luc Tg HL mice were established by crossing the Tg C57BL/6 mouse strain with the HL mouse strain. Under physiological and pathological conditions, BLI was performed to detect the signal intensity changes at various developmental stages and at an interval of <7 days. The established Arc-Luc Tg HL mice exhibited clear and stable photon signals from the brain without interference during development. After surgical monocular deprivation during visual-critical period, large signal intensity changes in bioluminescence were observed in the mouse visual cortex. Exposure of mice to a novel object changed the photon distribution in the caudal and rostral cerebral areas. The temporal pattern of kainic-acid-induced Arc-Luc expression showed biphasic changes in signal intensity over 24 h. CONCLUSIONS: This study showed the advantages of using the mutant HL gene in BLI of Arc expression in the mouse brain at various developmental stages. Thus, the use of the Arc-Luc Tg HL mice enabled the tracking of neuronal-activity-dependent processes over a wide range from a focal area to the entire brain area with various time windows.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Cytoskeletal Proteins); 0 (Excitatory Amino Acid Agonists); 0 (Nerve Tissue Proteins); 0 (Transcription Factors); 0 (activity regulated cytoskeletal-associated protein); 0 (hr protein, mouse); EC 1.13.12.7 (Luciferases, Firefly); SIV03811UC (Kainic Acid)


  7 / 890 MEDLINE  
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PMID:27728852
Autor:Dunn EC; Nishimi K; Powers A; Bradley B
Endereço:Psychiatric and Neurodevelopmental Genetics Unit, Massachusetts General Hospital, 185 Cambridge St, Simches Research Building, Boston, MA 02114, USA; Department of Psychiatry, Harvard Medical School, 401 Park Drive, 2 West, Room 305, Boston, MA 02215, USA; Stanley Center for Psychiatric Research, Th
Título:Is developmental timing of trauma exposure associated with depressive and post-traumatic stress disorder symptoms in adulthood?
Fonte:J Psychiatr Res; 84:119-127, 2017 Jan.
ISSN:1879-1379
País de publicação:England
Idioma:eng
Resumo:BACKGROUND: Trauma exposure is a known risk factor for psychopathology. However, the impact of the developmental timing of exposure remains unclear. This study examined the effect of age at first trauma exposure on levels of adult depressive and posttraumatic stress disorder (PTSD) symptoms. METHODS: Lifetime trauma exposure (including age at first exposure and frequency), current psychiatric symptoms, and sociodemographic information were collected during interviews with adults participating in a study at a public urban hospital in Atlanta, GA. Multiple linear regression models assessed the association between timing of first trauma exposure, classified as early childhood (ages 0-5), middle childhood (ages 6-10), adolescence (ages 11-18), and adulthood (ages 19+), on adult psychopathology in 2892 individuals. RESULTS: Participants exposed to trauma (i.e., child maltreatment, other interpersonal violence, non-interpersonal violence, and other events) at any age had higher depressive and PTSD symptoms compared to their unexposed peers. However, participants first exposed to child maltreatment during early childhood had depression and PTSD symptoms that were about twice as high as those exposed during later developmental stages. This association was detected even after controlling for sociodemographic characteristics, exposure to other trauma types, and frequency of exposure. Participants first exposed during middle childhood to other interpersonal violence also had depressive symptoms scores that were about twice as high as those first exposed during adulthood. CONCLUSIONS: Trauma exposure at different ages may differentially impact depressive and PTSD symptoms in adulthood. More detailed examination of timing of trauma exposure is warranted to aid in identifying sensitive periods in development.
Tipo de publicação: JOURNAL ARTICLE


  8 / 890 MEDLINE  
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PMID:27567276
Autor:Ismail FY; Fatemi A; Johnston MV
Endereço:Department of neurology and developmental medicine, The Kennedy Krieger Institute, Johns Hopkins Medical Institutions, MD, USA; Department of pediatrics, College of Medicine and Health Sciences, United Arab Emirates University, Al- Ain, UAE. Electronic address: fismail4@jhmi.edu.
Título:Cerebral plasticity: Windows of opportunity in the developing brain.
Fonte:Eur J Paediatr Neurol; 21(1):23-48, 2017 Jan.
ISSN:1532-2130
País de publicação:England
Idioma:eng
Resumo:BACKGROUND: Neuroplasticity refers to the inherently dynamic biological capacity of the central nervous system (CNS) to undergo maturation, change structurally and functionally in response to experience and to adapt following injury. This malleability is achieved by modulating subsets of genetic, molecular and cellular mechanisms that influence the dynamics of synaptic connections and neural circuitry formation culminating in gain or loss of behavior or function. Neuroplasticity in the healthy developing brain exhibits a heterochronus cortex-specific developmental profile and is heightened during "critical and sensitive periods" of pre and postnatal brain development that enable the construction and consolidation of experience-dependent structural and functional brain connections. PURPOSE: In this review, our primary goal is to highlight the essential role of neuroplasticity in brain development, and to draw attention to the complex relationship between different levels of the developing nervous system that are subjected to plasticity in health and disease. Another goal of this review is to explore the relationship between plasticity responses of the developing brain and how they are influenced by critical and sensitive periods of brain development. Finally, we aim to motivate researchers in the pediatric neuromodulation field to build on the current knowledge of normal and abnormal neuroplasticity, especially synaptic plasticity, and their dependence on "critical or sensitive periods" of neural development to inform the design, timing and sequencing of neuromodulatory interventions in order to enhance and optimize their translational applications in childhood disorders of the brain. METHODS: literature review. RESULTS: We discuss in details five patterns of neuroplasticity expressed by the developing brain: 1) developmental plasticity which is further classified into normal and impaired developmental plasticity as seen in syndromic autism spectrum disorders, 2) adaptive (experience-dependent) plasticity following intense motor skill training, 3) reactive plasticity to pre and post natal CNS injury or sensory deprivation, 4) excessive plasticity (loss of homeostatic regulation) as seen in dystonia and refractory epilepsy, 6) and finally, plasticity as the brain's "Achilles tendon" which induces brain vulnerability under certain conditions such as hypoxic ischemic encephalopathy and epileptic encephalopathy syndromes. We then explore the unique feature of "time-sensitive heightened plasticity responses" in the developing brain in the in the context of neuromodulation. CONCLUSION: The different patterns of neuroplasticity and the unique feature of heightened plasticity during critical and sensitive periods are important concepts for researchers and clinicians in the field of pediatric neurology and neurodevelopmental disabilities. These concepts need to be examined systematically in the context of pediatric neuromodulation. We propose that critical and sensitive periods of brain development in health and disease can create "windows of opportunity" for neuromodulatory interventions that are not commonly seen in adult brain and probably augment plasticity responses and improve clinical outcomes.
Tipo de publicação: JOURNAL ARTICLE; REVIEW


  9 / 890 MEDLINE  
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PMID:26728172
Autor:Tzanoulinou S; Sandi C
Endereço:Department of Fundamental Neurosciences, University of Lausanne, Rue Du Bugnon 9, CH-1005, Lausanne, Switzerland.
Título:The Programming of the Social Brain by Stress During Childhood and Adolescence: From Rodents to Humans.
Fonte:Curr Top Behav Neurosci; 30:411-429, 2017.
ISSN:1866-3370
País de publicação:Germany
Idioma:eng
Resumo:The quality and quantity of social experience is fundamental to an individual's health and well-being. Early life stress is known to be an important factor in the programming of the social brain that exerts detrimental effects on social behaviors. The peri-adolescent period, comprising late childhood and adolescence, represents a critical developmental window with regard to the programming effects of stress on the social brain. Here, we discuss social behavior and the physiological and neurobiological consequences of stress during peri-adolescence in the context of rodent paradigms that model human adversity, including social neglect and isolation, social abuse, and exposure to fearful experiences. Furthermore, we discuss peri-adolescent stress as a potent component that influences the social behaviors of individuals in close contact with stressed individuals and that can also influence future generations. We also discuss the temporal dynamics programmed by stress on the social brain and debate whether social behavior alterations are adaptive or maladaptive. By revising the existing literature and defining open questions, we aim to expand the framework in which interactions among peri-adolescent stress, the social brain, and behavior can be better conceptualized.
Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW


  10 / 890 MEDLINE  
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PMID:28101530
Autor:Smith MR; Burman P; Sadahiro M; Kidd BA; Dudley JT; Morishita H
Endereço:Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, New York 10029; Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, New York 10029; Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, New York 10029;
Título:Integrative Analysis of Disease Signatures Shows Inflammation Disrupts Juvenile Experience-Dependent Cortical Plasticity.
Fonte:eNeuro; 3(6), 2016 Nov-Dec.
ISSN:2373-2822
País de publicação:United States
Idioma:eng
Resumo:Throughout childhood and adolescence, periods of heightened neuroplasticity are critical for the development of healthy brain function and behavior. Given the high prevalence of neurodevelopmental disorders, such as autism, identifying disruptors of developmental plasticity represents an essential step for developing strategies for prevention and intervention. Applying a novel computational approach that systematically assessed connections between 436 transcriptional signatures of disease and multiple signatures of neuroplasticity, we identified inflammation as a common pathological process central to a diverse set of diseases predicted to dysregulate plasticity signatures. We tested the hypothesis that inflammation disrupts developmental cortical plasticity using the mouse ocular dominance model of experience-dependent plasticity in primary visual cortex. We found that the administration of systemic lipopolysaccharide suppressed plasticity during juvenile critical period with accompanying transcriptional changes in a particular set of molecular regulators within primary visual cortex. These findings suggest that inflammation may have unrecognized adverse consequences on the postnatal developmental trajectory and indicate that treating inflammation may reduce the burden of neurodevelopmental disorders.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Lipopolysaccharides); 0 (Lynx1 protein, mouse); 0 (Membrane Glycoproteins); 0 (Neuropeptides)



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