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  • 1
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    Stably maintained dendritic spines are associated with lifelong memories (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-12-01
    Description: Changes in synaptic connections are considered essential for learning and memory formation. However, it is unknown how neural circuits undergo continuous synaptic changes during learning while maintaining lifelong memories. Here we show, by following postsynaptic dendritic spines over time in the mouse cortex, that learning and novel sensory experience lead to spine formation and elimination by a protracted process. The extent of spine remodelling correlates with behavioural improvement after learning, suggesting a crucial role of synaptic structural plasticity in memory formation. Importantly, a small fraction of new spines induced by novel experience, together with most spines formed early during development and surviving experience-dependent elimination, are preserved and provide a structural basis for memory retention throughout the entire life of an animal. These studies indicate that learning and daily sensory experience leave minute but permanent marks on cortical connections and suggest that lifelong memories are stored in largely stably connected synaptic networks.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4724802/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4724802/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Guang -- Pan, Feng -- Gan, Wen-Biao -- R01 NS047325/NS/NINDS NIH HHS/ -- England -- Nature. 2009 Dec 17;462(7275):920-4. doi: 10.1038/nature08577. Epub 2009 Nov 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Neurobiology Program, The Helen and Martin Kimmel Center for Biology and Medicine at the Skirball Institute of Biomolecular Medicine, Department of Physiology and Neuroscience, New York University School of Medicine, New York, New York 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19946265" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/physiology ; Animals ; Dendritic Spines/metabolism/*physiology ; Forelimb/physiology ; Memory/*physiology ; Mice ; Motor Cortex/cytology/physiology ; Motor Skills/physiology ; Neuronal Plasticity/physiology ; Pyramidal Cells/metabolism ; Synapses/*metabolism ; Time Factors
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Sleep promotes branch-specific formation of dendritic spines after learning (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-06-07
    Description: How sleep helps learning and memory remains unknown. We report in mouse motor cortex that sleep after motor learning promotes the formation of postsynaptic dendritic spines on a subset of branches of individual layer V pyramidal neurons. New spines are formed on different sets of dendritic branches in response to different learning tasks and are protected from being eliminated when multiple tasks are learned. Neurons activated during learning of a motor task are reactivated during subsequent non-rapid eye movement sleep, and disrupting this neuronal reactivation prevents branch-specific spine formation. These findings indicate that sleep has a key role in promoting learning-dependent synapse formation and maintenance on selected dendritic branches, which contribute to memory storage.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4447313/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4447313/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Guang -- Lai, Cora Sau Wan -- Cichon, Joseph -- Ma, Lei -- Li, Wei -- Gan, Wen-Biao -- P01 NS074972/NS/NINDS NIH HHS/ -- R01 NS047325/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2014 Jun 6;344(6188):1173-8. doi: 10.1126/science.1249098.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Skirball Institute, Department of Neuroscience and Physiology, New York University School of Medicine, New York, NY 10016, USA. Department of Anesthesiology, New York University School of Medicine, New York, NY 10016, USA. ; Skirball Institute, Department of Neuroscience and Physiology, New York University School of Medicine, New York, NY 10016, USA. ; Skirball Institute, Department of Neuroscience and Physiology, New York University School of Medicine, New York, NY 10016, USA. Drug Discovery Center, Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, 518055, China. ; Drug Discovery Center, Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, 518055, China. ; Skirball Institute, Department of Neuroscience and Physiology, New York University School of Medicine, New York, NY 10016, USA. gan@saturn.med.nyu.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24904169" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dendritic Spines/*physiology ; Female ; Learning/*physiology ; Male ; Mice ; Mice, Mutant Strains ; Motor Cortex/*physiology ; Sleep, REM/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Synaptic segregation at the developing neuromuscular junction (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-11-20
    Description: Throughout the developing nervous system, competition between axons causes the permanent removal of some synaptic connections. In mouse neuromuscular junctions at birth, terminal branches of different axons are intermingled. However, during the several weeks after birth, these branches progressively segregated into nonoverlapping compartments before the complete withdrawal of all but one axon. Segregation was caused by selective branch atrophy, detachment, and withdrawal; the axon branches that were nearest to the competitor's branches were removed before the more distant branches were removed. This progression suggests that the signals that mediate the competitive removal of synapses must decrease in potency over short distances.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gan, W B -- Lichtman, J W -- New York, N.Y. -- Science. 1998 Nov 20;282(5393):1508-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Neurobiology, Washington University School of Medicine, 660 South Euclid Avenue, Box 8108, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9822385" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Axons/physiology/*ultrastructure ; Cytoskeleton/ultrastructure ; Fluorescent Dyes ; Mice ; Microscopy, Confocal ; Neuromuscular Junction/chemistry/*growth & development/*ultrastructure ; Presynaptic Terminals/physiology/*ultrastructure ; Receptors, Cholinergic/analysis ; Synapses/physiology/*ultrastructure
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    Branch-specific dendritic Ca(2+) spikes cause persistent synaptic plasticity (2015)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2015-03-31
    Description: The brain has an extraordinary capacity for memory storage, but how it stores new information without disrupting previously acquired memories remains unknown. Here we show that different motor learning tasks induce dendritic Ca(2+) spikes on different apical tuft branches of individual layer V pyramidal neurons in the mouse motor cortex. These task-related, branch-specific Ca(2+) spikes cause long-lasting potentiation of postsynaptic dendritic spines active at the time of spike generation. When somatostatin-expressing interneurons are inactivated, different motor tasks frequently induce Ca(2+) spikes on the same branches. On those branches, spines potentiated during one task are depotentiated when they are active seconds before Ca(2+) spikes induced by another task. Concomitantly, increased neuronal activity and performance improvement after learning one task are disrupted when another task is learned. These findings indicate that dendritic-branch-specific generation of Ca(2+) spikes is crucial for establishing long-lasting synaptic plasticity, thereby facilitating information storage associated with different learning experiences.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4476301/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4476301/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cichon, Joseph -- Gan, Wen-Biao -- P01 NS074972/NS/NINDS NIH HHS/ -- R01 NS047325/NS/NINDS NIH HHS/ -- England -- Nature. 2015 Apr 9;520(7546):180-5. doi: 10.1038/nature14251. Epub 2015 Mar 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Skirball Institute, Department of Neuroscience and Physiology, New York University School of Medicine, New York, New York 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25822789" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Calcium/*metabolism ; Calcium Signaling ; Dendrites/*metabolism ; Dendritic Spines/metabolism ; Female ; Interneurons/metabolism ; Long-Term Potentiation/physiology ; Male ; Memory/physiology ; Mice ; Motor Cortex/cytology/physiology ; *Neuronal Plasticity ; Psychomotor Performance/physiology ; Pyramidal Cells/metabolism ; Time Factors
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 5
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    Opposite effects of fear conditioning and extinction on dendritic spine remodelling (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-02-22
    Description: It is generally believed that fear extinction is a form of new learning that inhibits rather than erases previously acquired fear memories. Although this view has gained much support from behavioural and electrophysiological studies, the hypothesis that extinction causes the partial erasure of fear memories remains viable. Using transcranial two-photon microscopy, we investigated how neural circuits are modified by fear learning and extinction by examining the formation and elimination of postsynaptic dendritic spines of layer-V pyramidal neurons in the mouse frontal association cortex. Here we show that fear conditioning by pairing an auditory cue with a footshock increases the rate of spine elimination. By contrast, fear extinction by repeated presentation of the same auditory cue without a footshock increases the rate of spine formation. The degrees of spine remodelling induced by fear conditioning and extinction strongly correlate with the expression and extinction of conditioned fear responses, respectively. Notably, spine elimination and formation induced by fear conditioning and extinction occur on the same dendritic branches in a cue- and location-specific manner: cue-specific extinction causes formation of dendritic spines within a distance of two micrometres from spines that were eliminated after fear conditioning. Furthermore, reconditioning preferentially induces elimination of dendritic spines that were formed after extinction. Thus, within vastly complex neuronal networks, fear conditioning, extinction and reconditioning lead to opposing changes at the level of individual synapses. These findings also suggest that fear memory traces are partially erased after extinction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lai, Cora Sau Wan -- Franke, Thomas F -- Gan, Wen-Biao -- NS047325/NS/NINDS NIH HHS/ -- England -- Nature. 2012 Feb 19;483(7387):87-91. doi: 10.1038/nature10792.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Neurobiology Program, Skirball Institute, Department of Physiology and Neuroscience, New York University School of Medicine, 540 First Avenue, New York, New York 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22343895" target="_blank"〉PubMed〈/a〉
    Keywords: Acoustic Stimulation ; Animals ; Conditioning, Classical/*physiology ; Cues ; Dendritic Spines/*physiology ; Electric Stimulation ; Extinction, Psychological/*physiology ; Extremities ; Fear/*physiology ; Frontal Lobe/cytology/physiology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Models, Neurological ; Neuronal Plasticity/*physiology ; Pyramidal Cells/cytology/physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 6
    Electronic Resource
    Electronic Resource
    Total factor productivity growth in the Singapore manufacturing industries during the 1980's
    Amsterdam : Elsevier
    Journal of Asian Economics 5 (1994), S. 177-196 
    Details
    ISSN: 1049-0078
    Keywords: [JEL classification codes] O47
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Economics
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/1049-0078(94)90023-X
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    Paper (German National Licenses)
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  • 7
    Electronic Resource
    Electronic Resource
    Rational expectations, saving and anticipated changes in income: Evidence from Malaysia and Singapore
    Amsterdam : Elsevier
    Journal of Macroeconomics 16 (1994), S. 157-170 
    Details
    ISSN: 0164-0704
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Economics
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/0164-0704(94)90049-3
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  • 8
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    Peripheral elevation of TNF-  leads to early synaptic abnormalities in the mouse somatosensory cortex in experimental autoimmune encephalomyelitis (2013)
    National Academy of Sciences
    Details
    Publication Date: 2013-06-03
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 9
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    Glucocorticoids are critical regulators of dendritic spine development and plasticity in vivo (2011)
    National Academy of Sciences
    Details
    Publication Date: 2011-09-12
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 10
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    Glucocorticoids are critical regulators of dendritic spine development and plasticity in vivo [Neuroscience] (2011)
    National Academy of Sciences
    Details
    Publication Date: 2011-09-21
    Description: Glucocorticoids are a family of hormones that coordinate diverse physiological processes in responding to stress. Prolonged glucocorticoid exposure over weeks has been linked to dendritic atrophy and spine loss in fixed tissue studies of adult brains, but it is unclear how glucocorticoids may affect the dynamic processes of dendritic spine formation and elimination in vivo. Furthermore, relatively few studies have examined the effects of stress and glucocorticoids on spines during the postnatal and adolescent period, which is characterized by rapid synaptogenesis followed by protracted synaptic pruning. To determine whether and to what extent glucocorticoids regulate dendritic spine development and plasticity, we used transcranial two-photon microscopy to track the formation and elimination of dendritic spines in vivo after treatment with glucocorticoids in developing and adult mice. Corticosterone, the principal murine glucocorticoid, had potent dose-dependent effects on dendritic spine dynamics, increasing spine turnover within several hours in the developing barrel cortex. The adult barrel cortex exhibited diminished baseline spine turnover rates, but these rates were also enhanced by corticosterone. Similar changes occurred in multiple cortical areas, suggesting a generalized effect. However, reducing endogenous glucocorticoid activity by dexamethasone suppression or corticosteroid receptor antagonists caused a substantial reduction in spine turnover rates, and the former was reversed by corticosterone replacement. Notably, we found that chronic glucocorticoid excess led to an abnormal loss of stable spines that were established early in life. Together, these findings establish a critical role for glucocorticoids in the development and maintenance of dendritic spines in the living cortex.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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