For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
80
views
131
references
 Top references
cited by
156
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      175
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Mitochondria and neuroplasticity

      review-article
      Author(s): * , 1 , * , * , † , 1
      Publication date (Electronic):
      Journal: ASN NEURO
      Publisher: American Society for Neurochemistry
      Keywords: neural progenitor cell, mitochondria biogenesis, mitochondria fission and fusion, Aβ, amyloid β-peptide, AD, Alzheimer's disease, AP, adaptor protein, APP, amyloid precursor protein, BDNF, brain-derived neurotrophic factor, CaMK, Ca2+/calmodulin-dependent protein kinase, CR, caloric restriction, CREB, cAMP-response-element-binding protein, ES, embryonic stem, ETC, electron transport chain, HD, Huntington's disease, LRRK2, leucine-rich repeat kinase 2, LTP, long-term potentiation, MAPK, mitogen-activated protein kinase, Mn-SOD, manganese superoxide dismutase, NGF, nerve growth factor, NMDA, N-methyl-d-aspartate, Nrf1, nuclear respiratory factor 1, OPA1, Optic Atrophy-1, PD, Parkinson's disease, PGC1α, peroxisome-proliferator-activated receptor γ co-activator 1α, PINK1, PTEN (phosphatase and tensin homologue deleted on chromosome 10)-induced kinase 1 , PPAR, peroxisome-proliferator-activated receptor, UCP, uncoupling protein

      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

          The production of neurons from neural progenitor cells, the growth of axons and dendrites and the formation and reorganization of synapses are examples of neuroplasticity. These processes are regulated by cell-autonomous and intercellular (paracrine and endocrine) programs that mediate responses of neural cells to environmental input. Mitochondria are highly mobile and move within and between subcellular compartments involved in neuroplasticity (synaptic terminals, dendrites, cell body and the axon). By generating energy (ATP and NAD +), and regulating subcellular Ca 2+ and redox homoeostasis, mitochondria may play important roles in controlling fundamental processes in neuroplasticity, including neural differentiation, neurite outgrowth, neurotransmitter release and dendritic remodelling. Particularly intriguing is emerging data suggesting that mitochondria emit molecular signals (e.g. reactive oxygen species, proteins and lipid mediators) that can act locally or travel to distant targets including the nucleus. Disturbances in mitochondrial functions and signalling may play roles in impaired neuroplasticity and neuronal degeneration in Alzheimer's disease, Parkinson's disease, psychiatric disorders and stroke.

          Related collections

          Most cited references131

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

          Running enhances neurogenesis, learning, and long-term potentiation in mice.

          H. van Praag, B R Christie, T J Sejnowski … (1999)
          Running increases neurogenesis in the dentate gyrus of the hippocampus, a brain structure that is important for memory function. Consequently, spatial learning and long-term potentiation (LTP) were tested in groups of mice housed either with a running wheel (runners) or under standard conditions (controls). Mice were injected with bromodeoxyuridine to label dividing cells and trained in the Morris water maze. LTP was studied in the dentate gyrus and area CA1 in hippocampal slices from these mice. Running improved water maze performance, increased bromodeoxyuridine-positive cell numbers, and selectively enhanced dentate gyrus LTP. Our results indicate that physical activity can regulate hippocampal neurogenesis, synaptic plasticity, and learning.
          Article 0 comments Cited 318 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Astrocyte control of synaptic transmission and neurovascular coupling.

            Philip Haydon, Giorgio Carmignoto (2006)
            From a structural perspective, the predominant glial cell of the central nervous system, the astrocyte, is positioned to regulate synaptic transmission and neurovascular coupling: the processes of one astrocyte contact tens of thousands of synapses, while other processes of the same cell form endfeet on capillaries and arterioles. The application of subcellular imaging of Ca2+ signaling to astrocytes now provides functional data to support this structural notion. Astrocytes express receptors for many neurotransmitters, and their activation leads to oscillations in internal Ca2+. These oscillations induce the accumulation of arachidonic acid and the release of the chemical transmitters glutamate, d-serine, and ATP. Ca2+ oscillations in astrocytic endfeet can control cerebral microcirculation through the arachidonic acid metabolites prostaglandin E2 and epoxyeicosatrienoic acids that induce arteriole dilation, and 20-HETE that induces arteriole constriction. In addition to actions on the vasculature, the release of chemical transmitters from astrocytes regulates neuronal function. Astrocyte-derived glutamate, which preferentially acts on extrasynaptic receptors, can promote neuronal synchrony, enhance neuronal excitability, and modulate synaptic transmission. Astrocyte-derived d-serine, by acting on the glycine-binding site of the N-methyl-d-aspartate receptor, can modulate synaptic plasticity. Astrocyte-derived ATP, which is hydrolyzed to adenosine in the extracellular space, has inhibitory actions and mediates synaptic cross-talk underlying heterosynaptic depression. Now that we appreciate this range of actions of astrocytic signaling, some of the immediate challenges are to determine how the astrocyte regulates neuronal integration and how both excitatory (glutamate) and inhibitory signals (adenosine) provided by the same glial cell act in concert to regulate neuronal function.
            Article 0 comments Cited 286 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Mitochondrial dynamics in mammalian health and disease.

              Marc Liesa, Manuel Palacín, Antonio Zorzano (2009)
              The meaning of the word mitochondrion (from the Greek mitos, meaning thread, and chondros, grain) illustrates that the heterogeneity of mitochondrial morphology has been known since the first descriptions of this organelle. Such a heterogeneous morphology is explained by the dynamic nature of mitochondria. Mitochondrial dynamics is a concept that includes the movement of mitochondria along the cytoskeleton, the regulation of mitochondrial architecture (morphology and distribution), and connectivity mediated by tethering and fusion/fission events. The relevance of these events in mitochondrial and cell physiology has been partially unraveled after the identification of the genes responsible for mitochondrial fusion and fission. Furthermore, during the last decade, it has been identified that mutations in two mitochondrial fusion genes (MFN2 and OPA1) cause prevalent neurodegenerative diseases (Charcot-Marie Tooth type 2A and Kjer disease/autosomal dominant optic atrophy). In addition, other diseases such as type 2 diabetes or vascular proliferative disorders show impaired MFN2 expression. Altogether, these findings have established mitochondrial dynamics as a consolidated area in cellular physiology. Here we review the most significant findings in the field of mitochondrial dynamics in mammalian cells and their implication in human pathologies.
              Article 0 comments Cited 285 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (nlm-ta): ASN Neuro
                Journal ID (publisher-id): ASN
                Title: ASN NEURO
                Publisher: American Society for Neurochemistry (9037 Ron Den Lane, Windermere, FL 34786 )
                ISSN (Electronic): 1759-0914
                Publication date (Electronic preprint): 13 August 2010
                Publication date (Electronic): 4 October 2010
                Publication date Collection: 2010
                Volume: 2
                Issue: 5
                Electronic Location Identifier: e00045
                Affiliations
                [1]*Laboratory of Neurosciences, National Institute of Aging Intramural Research Program, Baltimore, MD 21224, U.S.A.
                [2]†Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, U.S.A.
                Author notes
                1Correspondence may be addressed to either of these authors (email chengai@ 123456mail.nih.gov or mattsonm@ 123456grc.nia.nih.gov ).
                Article
                Publisher ID: e00045
                DOI: 10.1042/AN20100019
                PMC ID: 2949087
                PubMed ID: 20957078
                SO-VID: 09017667-96f7-4f2a-a75d-a268b2695dfe
                Copyright © © 2010 The Author(s).
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial Licence ( http://creativecommons.org/licenses/by-nc/2.5/) which permits unrestricted non-commercial use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 16 June 2010
                Date revision received : 6 August 2010
                Date accepted : 13 August 2010
                Categories
                Subject: Review Article
                Subject: S2

                ScienceOpen disciplines: Neurosciences
                Keywords: es, embryonic stem,camk, ca2+/calmodulin-dependent protein kinase,ad, alzheimer's disease,pgc1α, peroxisome-proliferator-activated receptor γ co-activator 1α,hd, huntington's disease,ap, adaptor protein,mn-sod, manganese superoxide dismutase,aβ, amyloid β-peptide,mitochondria biogenesis,app, amyloid precursor protein,pink1, pten (phosphatase and tensin homologue deleted on chromosome 10)-induced kinase 1,bdnf, brain-derived neurotrophic factor,mapk, mitogen-activated protein kinase,pd, parkinson's disease,ltp, long-term potentiation,ngf, nerve growth factor,neural progenitor cell,ppar, peroxisome-proliferator-activated receptor,cr, caloric restriction,nrf1, nuclear respiratory factor 1,lrrk2, leucine-rich repeat kinase 2,ucp, uncoupling protein,etc, electron transport chain,mitochondria fission and fusion,creb, camp-response-element-binding protein,nmda, n-methyl-d-aspartate,opa1, optic atrophy-1
                Data availability:
                ScienceOpen disciplines: Neurosciences
                Keywords: es, embryonic stem, camk, ca2+/calmodulin-dependent protein kinase, ad, alzheimer's disease, pgc1α, peroxisome-proliferator-activated receptor γ co-activator 1α, hd, huntington's disease, ap, adaptor protein, mn-sod, manganese superoxide dismutase, aβ, amyloid β-peptide, mitochondria biogenesis, app, amyloid precursor protein, pink1, pten (phosphatase and tensin homologue deleted on chromosome 10)-induced kinase 1, bdnf, brain-derived neurotrophic factor, mapk, mitogen-activated protein kinase, pd, parkinson's disease, ltp, long-term potentiation, ngf, nerve growth factor, neural progenitor cell, ppar, peroxisome-proliferator-activated receptor, cr, caloric restriction, nrf1, nuclear respiratory factor 1, lrrk2, leucine-rich repeat kinase 2, ucp, uncoupling protein, etc, electron transport chain, mitochondria fission and fusion, creb, camp-response-element-binding protein, nmda, n-methyl-d-aspartate, opa1, optic atrophy-1

                Comments

                Comment on this article

                scite_

                Similar content175

                See all similar

                Cited by150

                See all cited by

                Most referenced authors2,245

                See all reference authors