For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
5
views
41
references
 Top references
cited by
49
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      287
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      CREB controls cortical circuit plasticity and functional recovery after stroke

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Treatments that stimulate neuronal excitability enhance motor performance after stroke. cAMP-response-element binding protein (CREB) is a transcription factor that plays a key role in neuronal excitability. Increasing the levels of CREB with a viral vector in a small pool of motor neurons enhances motor recovery after stroke, while blocking CREB signaling prevents stroke recovery. Silencing CREB-transfected neurons in the peri-infarct region with the hM4Di-DREADD blocks motor recovery. Reversing this inhibition allows recovery to continue, demonstrating that by manipulating the activity of CREB-transfected neurons it is possible to turn off and on stroke recovery. CREB transfection enhances remapping of injured somatosensory and motor circuits, and induces the formation of new connections within these circuits. CREB is a central molecular node in the circuit responses after stroke that lead to recovery from motor deficits.

          Abstract

          Increasing excitability in the peri-infarct area enhances motor recovery after stroke. Here the authors show that expressing CREB, a transcription factor known for its role in synaptic plasticity, or increasing activity of CREB-expressing cells near the stroke site improves recovery in an effect that is strong enough that it can be used to turn on and off motor recovery after stroke.

          Related collections

          Most cited references41

          • Record: found
          • Abstract: found
          • Article: not found

          Modulation of brain plasticity in stroke: a novel model for neurorehabilitation.

          Giovanni Di Pino, Giovanni Pellegrino, Giovanni Assenza … (2014)
          Noninvasive brain stimulation (NIBS) techniques can be used to monitor and modulate the excitability of intracortical neuronal circuits. Long periods of cortical stimulation can produce lasting effects on brain function, paving the way for therapeutic applications of NIBS in chronic neurological disease. The potential of NIBS in stroke rehabilitation has been of particular interest, because stroke is the main cause of permanent disability in industrial nations, and treatment outcomes often fail to meet the expectations of patients. Despite promising reports from many clinical trials on NIBS for stroke recovery, the number of studies reporting a null effect remains a concern. One possible explanation is that the interhemispheric competition model--which posits that suppressing the excitability of the hemisphere not affected by stroke will enhance recovery by reducing interhemispheric inhibition of the stroke hemisphere, and forms the rationale for many studies--is oversimplified or even incorrect. Here, we critically review the proposed mechanisms of synaptic and functional reorganization after stroke, and suggest a bimodal balance-recovery model that links interhemispheric balancing and functional recovery to the structural reserve spared by the lesion. The proposed model could enable NIBS to be tailored to the needs of individual patients.
          Article 0 comments Cited 315 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Repairing the human brain after stroke: I. Mechanisms of spontaneous recovery.

            Steven Cramer (2008)
            Stroke remains a leading cause of adult disability. Some degree of spontaneous behavioral recovery is usually seen in the weeks after stroke onset. Variability in recovery is substantial across human patients. Some principles have emerged; for example, recovery occurs slowest in those destined to have less successful outcomes. Animal studies have extended these observations, providing insight into a broad range of underlying molecular and physiological events. Brain mapping studies in human patients have provided observations at the systems level that often parallel findings in animals. In general, the best outcomes are associated with the greatest return toward the normal state of brain functional organization. Reorganization of surviving central nervous system elements supports behavioral recovery, for example, through changes in interhemispheric lateralization, activity of association cortices linked to injured zones, and organization of cortical representational maps. A number of factors influence events supporting stroke recovery, such as demographics, behavioral experience, and perhaps genetics. Such measures gain importance when viewed as covariates in therapeutic trials of restorative agents that target stroke recovery.
            Article 0 comments Cited 243 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Postsynaptic receptor trafficking underlying a form of associative learning.

              Simon Rumpel, Joseph LeDoux, Anthony Zador … (2005)
              To elucidate molecular, cellular, and circuit changes that occur in the brain during learning, we investigated the role of a glutamate receptor subtype in fear conditioning. In this form of learning, animals associate two stimuli, such as a tone and a shock. Here we report that fear conditioning drives AMPA-type glutamate receptors into the synapse of a large fraction of postsynaptic neurons in the lateral amygdala, a brain structure essential for this learning process. Furthermore, memory was reduced if AMPA receptor synaptic incorporation was blocked in as few as 10 to 20% of lateral amygdala neurons. Thus, the encoding of memories in the lateral amygdala is mediated by AMPA receptor trafficking, is widely distributed, and displays little redundancy.
              Article 0 comments Cited 185 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                S. T. Carmichael:
                ORCID: http://orcid.org/0000-0002-1169-9203
                scarmichael@mednet.ucla.edu
                Journal
                Journal ID (nlm-ta): Nat Commun
                Journal ID (iso-abbrev): Nat Commun
                Title: Nature Communications
                Publisher: Nature Publishing Group UK (London )
                ISSN (Electronic): 2041-1723
                Publication date (Electronic): 8 June 2018
                Publication date PMC-release: 8 June 2018
                Publication date Collection: 2018
                Volume: 9
                Electronic Location Identifier: 2250
                Affiliations
                [1 ]ISNI 0000 0000 9632 6718, GRID grid.19006.3e, Department of Neurology, David Geffen School of Medicine, , University of California Los Angeles, ; Los Angeles, CA 90095 USA
                [2 ]ISNI 0000 0000 9632 6718, GRID grid.19006.3e, Department of Neurobiology, David Geffen School of Medicine, , University of California Los Angeles, ; Los Angeles, CA 90095 USA
                [3 ]ISNI 0000 0000 9632 6718, GRID grid.19006.3e, Department of Psychology, David Geffen School of Medicine, , University of California Los Angeles, ; Los Angeles, CA 90095 USA
                [4 ]ISNI 0000 0000 9632 6718, GRID grid.19006.3e, Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine, , University of California Los Angeles, ; Los Angeles, CA 90095 USA
                [5 ]ISNI 0000 0000 9632 6718, GRID grid.19006.3e, Integrative Center for Learning and Memory, David Geffen School of Medicine, , University of California Los Angeles, ; Los Angeles, CA 90095 USA
                [6 ]ISNI 0000 0000 9632 6718, GRID grid.19006.3e, Brain Research Institute, David Geffen School of Medicine, , University of California Los Angeles, ; Los Angeles, CA 90095 USA
                [7 ]ISNI 0000 0000 9632 6718, GRID grid.19006.3e, Program in Neurogenetics, Department of Neurology, David Geffen School of Medicine, , University of California Los Angeles, ; Los Angeles, CA 90095 USA
                [8 ]ISNI 0000 0000 9632 6718, GRID grid.19006.3e, Department of Psychiatry, Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine, , University of California Los Angeles, ; Los Angeles, CA 90095 USA
                Author information
                http://orcid.org/0000-0003-2105-1061
                http://orcid.org/0000-0002-1169-9203
                Article
                Publisher ID: 4445
                DOI: 10.1038/s41467-018-04445-9
                PMC ID: 5993731
                PubMed ID: 29884780
                SO-VID: 64de0063-8866-431a-b717-eb9424d4aa93
                Copyright © © The Author(s) 2018
                License:

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 9 March 2018
                Date accepted : 27 April 2018
                Categories
                Subject: Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2018

                ScienceOpen disciplines: Uncategorized
                Data availability:
                ScienceOpen disciplines: Uncategorized

                Comments

                Comment on this article

                scite_

                Similar content287

                See all similar

                Cited by49

                See all cited by

                Most referenced authors728

                See all reference authors