22
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      IGF-I: A Key Growth Factor that Regulates Neurogenesis and Synaptogenesis from Embryonic to Adult Stages of the Brain

      review-article

      Read this article at

      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 generation of neurons in the adult mammalian brain requires the activation of quiescent neural stem cells (NSCs). This activation and the sequential steps of neuron formation from NSCs are regulated by a number of stimuli, which include growth factors. Insulin-like growth factor-I (IGF-I) exert pleiotropic effects, regulating multiple cellular processes depending on their concentration, cell type, and the developmental stage of the animal. Although IGF-I expression is relatively high in the embryonic brain its levels drop sharply in the adult brain except in neurogenic regions, i.e., the hippocampus (HP) and the subventricular zone-olfactory bulb (SVZ-OB). By contrast, the expression of IGF-IR remains relatively high in the brain irrespective of the age of the animal. Evidence indicates that IGF-I influences NSC proliferation and differentiation into neurons and glia as well as neuronal maturation including synapse formation. Furthermore, recent studies have shown that IGF-I not only promote adult neurogenesis by regulating NSC number and differentiation but also by influencing neuronal positioning and migration as described during SVZ-OB neurogenesis. In this article we will revise and discuss the actions reported for IGF-I signaling in a variety of in vitro and in vivo models, focusing on the maintenance and proliferation of NSCs/progenitors, neurogenesis, and neuron integration in synaptic circuits.

          Related collections

          Most cited references97

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

          Mice carrying null mutations of the genes encoding insulin-like growth factor I (Igf-1) and type 1 IGF receptor (Igf1r).

          Newborn mice homozygous for a targeted disruption of insulin-like growth factor gene (Igf-1) exhibit a growth deficiency similar in severity to that previously observed in viable Igf-2 null mutants (60% of normal birthweight). Depending on genetic background, some of the Igf-1(-/-) dwarfs die shortly after birth, while others survive and reach adulthood. In contrast, null mutants for the Igf1r gene die invariably at birth of respiratory failure and exhibit a more severe growth deficiency (45% normal size). In addition to generalized organ hypoplasia in Igf1r(-/-) embryos, including the muscles, and developmental delays in ossification, deviations from normalcy were observed in the central nervous system and epidermis. Igf-1(-/-)/Igf1r(-/-) double mutants did not differ in phenotype from Igf1r(-/-) single mutants, while in Igf-2(-)/Igf1r(-/-) and Igf-1(-/-)/Igf-2(-) double mutants, which are phenotypically identical, the dwarfism was further exacerbated (30% normal size). The roles of the IGFs in mouse embryonic development, as revealed from the phenotypic differences between these mutants, are discussed.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Role of insulin-like growth factors in embryonic and postnatal growth.

            A developmental analysis of growth kinetics in mouse embryos carrying null mutations of the genes encoding insulin-like growth factor I (IGF-I), IGF-II, and the type 1 IGF receptor (IGF1R), alone or in combination, defined the onset of mutational effects leading to growth deficiency and indicated that between embryonic days 11.0 and 12.5, IGF1R serves only the in vivo mitogenic signaling of IGF-II. From E13.5 onward, IGF1R interacts with both IGF-I and IGF-II, while IGF-II recognizes an additional unknown receptor (XR). In contrast with the embryo proper, placental growth is served exclusively by an IGF-II-XR interaction. Additional genetic data suggested that the type 2IGF/mannose 6-phosphate receptor is an unlikely candidate for XR. Postnatal growth curves indicated that surviving Igf-1(-/-) mutants, which are infertile and exhibit delayed bone development, continue to grow with a retarded rate after birth in comparison with wild-type littermates and become 30% of normal weight as adults.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              The many faces of insulin-like peptide signalling in the brain.

              Central and peripheral insulin-like peptides (ILPs), which include insulin, insulin-like growth factor 1 (IGF1) and IGF2, exert many effects in the brain. Through their actions on brain growth and differentiation, ILPs contribute to building circuitries that subserve metabolic and behavioural adaptation to internal and external cues of energy availability. In the adult brain each ILP has distinct effects, but together their actions ultimately regulate energy homeostasis - they affect nutrient sensing and regulate neuronal plasticity to modulate adaptive behaviours involved in food seeking, including high-level cognitive operations such as spatial memory. In essence, the multifaceted activity of ILPs in the brain may be viewed as a system organization involved in the control of energy allocation.
                Bookmark

                Author and article information

                Contributors
                Journal
                Front Neurosci
                Front Neurosci
                Front. Neurosci.
                Frontiers in Neuroscience
                Frontiers Media S.A.
                1662-4548
                1662-453X
                23 February 2016
                2016
                : 10
                : 52
                Affiliations
                [1] 1Consejo Superior de Investigaciones Científicas (CSIC), Instituto Cajal Madrid, Spain
                [2] 2Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED) Madrid, Spain
                Author notes

                Edited by: Alino Martinez-Marcos, Universidad de Castilla, Spain

                Reviewed by: Jacques Epelbaum, Centre de Psychiatrie & Neurosciences, Université Paris Descartes, France; Jessica H. Brann, Loyola University Chicago, USA

                *Correspondence: Carlos Vicario-Abejón cvicario@ 123456cajal.csic.es

                This article was submitted to Neurogenesis, a section of the journal Frontiers in Neuroscience

                Article
                10.3389/fnins.2016.00052
                4763060
                26941597
                531a5de4-2b89-47fe-9ad6-172736e3856e
                Copyright © 2016 Nieto-Estévez, Defterali and Vicario-Abejón.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 07 December 2015
                : 05 February 2016
                Page count
                Figures: 1, Tables: 1, Equations: 0, References: 115, Pages: 9, Words: 7929
                Funding
                Funded by: Ministerio de Economía y Competitividad 10.13039/501100003329
                Award ID: SAF2013-4759R
                Funded by: Consejería de Sanidad, Comunidad de Madrid 10.13039/501100006541
                Award ID: S2011/BMD-2336
                Funded by: Instituto de Salud Carlos III 10.13039/501100004587
                Award ID: CIBERNED CB06/05/0065
                Categories
                Neuroscience
                Review

                Neurosciences
                igf-i,neurogenesis,proliferation,survival,differentiation,maturation,migration,igf-ir
                Neurosciences
                igf-i, neurogenesis, proliferation, survival, differentiation, maturation, migration, igf-ir

                Comments

                Comment on this article