Localization of insulin-like growth factor-1 mRNA in murine central nervous system during postnatal development

Bartlett, Will; Li, X.-S.; Williams, M. J.; Benkovic, S.J.

doi:10.1016/s0012-1606(05)80021-1

Cited by 138 publications

(85 citation statements)

References 40 publications

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“…In the early postnatal cerebellum, there are two sources of IGF-1: (i) serum IGF-1 secreted from the liver, which crosses the blood-brain barrier and enters the cerebellum (24), and (ii) IGF-1 produced locally within the cerebellum, which is synthesized primarily by Purkinje cells (25). In cerebellar microexplant cultures, the addition of the IGF-1 receptor inhibitor PPP to the cultures did not alter the speed of granule cell migration (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…Circulating IGF-1 crosses the blood-brain barrier easily, so cerebellar IGF-1 levels vary in parallel with serum IGF-1 levels (24). IGF-1 also is synthesized in the developing cerebellum (25). For example, Purkinje cells produce IGF-1 during the first two postnatal weeks (25).…”

Section: Light Stimuli Control Cerebellar and Serum Insulin-like Growthmentioning

confidence: 99%

“…IGF-1 also is synthesized in the developing cerebellum (25). For example, Purkinje cells produce IGF-1 during the first two postnatal weeks (25). Many neurons, including cerebellar granule cells, express IGF-1 receptors before the initiation of migration (26)(27)(28).…”

Section: Light Stimuli Control Cerebellar and Serum Insulin-like Growthmentioning

confidence: 99%

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Light stimuli control neuronal migration by altering of insulin-like growth factor 1 (IGF-1) signaling

Liu

Komuro

Fahrion

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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The role of genetic inheritance in brain development has been well characterized, but little is known about the contributions of natural environmental stimuli, such as the effect of light-dark cycles, to brain development. In this study, we determined the role of light stimuli in neuronal cell migration to elucidate how environmental factors regulate brain development. We show that in early postnatal mouse cerebella, granule cell migration accelerates during light cycles and decelerates during dark cycles. Furthermore, cerebellar levels of insulin-like growth factor 1 (IGF-1) are high during light cycles and low during dark cycles. There are causal relationships between light-dark cycles, speed of granule cell migration, and cerebellar IGF-1 levels. First, changes in lightdark cycles result in corresponding changes in the fluctuations of both speed of granule cell migration and cerebellar IGF-1 levels. Second, in vitro studies indicate that exogenous IGF-1 accelerates the migration of isolated granule cells through the activation of IGF-1 receptors. Third, in vivo studies reveal that inhibiting the IGF-1 receptors decelerates granule cell migration during light cycles (high IGF-1 levels) but does not alter migration during dark cycles (low IGF-1 levels). In contrast, stimulating the IGF-1 receptors accelerates granule cell migration during dark cycles (low IGF-1 levels) but does not alter migration during light cycles (high IGF-1 levels). These results suggest that during early postnatal development light stimuli control granule cell migration by altering the activity of IGF-1 receptors through modification of cerebellar IGF-1 levels. cerebellar granule cells | light stimulation

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Section: Discussionmentioning

confidence: 99%

Section: Light Stimuli Control Cerebellar and Serum Insulin-like Growthmentioning

confidence: 99%

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Light stimuli control neuronal migration by altering of insulin-like growth factor 1 (IGF-1) signaling

Liu

Komuro

Fahrion

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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“…Insulin-induced stimulation of glycogen synthesis in liver and muscle involves the phosphorylation of glycogen synthase kinase 3␤ (GSK3␤) on serine 9 (28,29). This phosphorylation prevents GSK3␤-induced inhibition of glycogen synthase, thus promoting glycogen synthesis.…”

Section: Molecular Mechanisms Of Igf1 Action In Brain Metabolismmentioning

confidence: 99%

“…Very little insulin is synthesized within the brain (4) and little circulating insulin crosses the blood-brain barrier (5). However, insulin-like growth factor 1 (Igf1), an insulin homologue, is abundant in the developing brain (6), where it is concentrated in large projection neurons (7)(8)(9). Igf1 and insulin receptors are also homologous, with nearly identical signal-transducing domains engaging many of the same intracellular pathways (10).…”

mentioning

confidence: 99%

Insulin-like growth factor 1 regulates developing brain glucose metabolism

Cheng

Reinhardt

Lee

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

185

113

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The brain has enormous anabolic needs during early postnatal development. This study presents multiple lines of evidence showing that endogenous brain insulin-like growth factor 1 (Igf1) serves an essential, insulin-like role in promoting neuronal glucose utilization and growth during this period. Brain 2-deoxy-D-[1-14 C]glucose uptake parallels Igf1 expression in wild-type mice and is profoundly reduced in Igf1؊͞؊ mice, particularly in those structures where Igf1 is normally most highly expressed. 2-Deoxy-D-[1-14 C]glucose is significantly reduced in synaptosomes prepared from Igf1؊͞؊ brains, and the deficit is corrected by inclusion of Igf1 in the incubation medium. The serine͞threonine kinase Akt͞ PKB is a major target of insulin-signaling in the regulation of glucose transport via the facilitative glucose transporter (GLUT4) and glycogen synthesis in peripheral tissues. Phosphorylation of Akt and GLUT4 expression are reduced in Igf1؊͞؊ neurons. Phosphorylation of glycogen synthase kinase 3␤ and glycogen accumulation also are reduced in Igf1؊͞؊ neurons. These data support the hypothesis that endogenous brain Igf1 serves an anabolic, insulin-like role in developing brain metabolism.mental retardation ͉ glycogen synthase kinase ͉ glucose transporter ͉ GLUT4 ͉ Akt T he brain requires enormous supplies of fuel to support neuroglial growth and process formation during early postnatal development. Murine and human brains consume over half the energy available to the organism as a whole during this critical period (1), when undernutrition may result in permanent intellectual deficit (2). How the developing brain competes so successfully with peripheral tissues for resources is unknown. Insulin preferentially enhances fuel and substrate utilization by peripheral tissues, but does not seem to be involved in the regulation of brain metabolism (3). Very little insulin is synthesized within the brain (4) and little circulating insulin crosses the blood-brain barrier (5). However, insulin-like growth factor 1 (Igf1), an insulin homologue, is abundant in the developing brain (6), where it is concentrated in large projection neurons (7-9). Igf1 and insulin receptors are also homologous, with nearly identical signal-transducing domains engaging many of the same intracellular pathways (10). The Igf1 receptor (Igf1R) is widely expressed in the brain (11)(12)(13)(14) where it is most abundant in Igf1-expressing neurons (15), suggesting a local autocrine͞paracrine mode of action for neuronal Igf1. Although Igf1's precise role in brain development is unknown, its importance seems clear because IGF1 gene deletion in humans results in mental retardation (16). Based on Igf1͞Igf1R expression patterns in the developing brain and on the functional homology with the insulin͞insulin receptor dyad, we hypothesized that neuronal Igf1 serves an anabolic, literally ''insulin-like'' role in brain development (17). To test this hypothesis, we investigated glucose utilization in Igf1-targeted gene deletion mice. Experimental ProceduresThe mice ...

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In vivo actions of fibroblast growth factor-2 and insulin-like growth factor-I on oligodendrocyte development and myelination in the central nervous system

1999

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The in vivo effects of fibroblast growth factor-2 (FGF-2) and insulin-like growth factor-I (IGF-I) on oligodendrocytes and CNS myelination were determined in the postnatal rat anterior medullary velum (AMV) following injection of both cytokines into the cerebrospinal fluid. Either FGF-2, IGF-I, or saline were administered via the lateral ventricle, twice daily commencing at postnatal day (P) 6. At P9, AMV were immunohistochemically labeled with the Rip antibody, to enable analysis of the numbers of myelin sheaths and of promyelinating and myelinating oligodendrocytes; promyelinating oligodendrocytes are a recognisable immature phenotype which express myelin-related proteins prior to forming myelin sheaths. In parallel experiments, AMV were treated for Western blot analysis to determine relative changes in expression of the myelin proteins 2', 3'-cyclic nucleotide 3'-phosphohydrolase (CNP) and myelin oligodendrocyte glycoprotein (MOG), which, respectively, characterise early and late stages of myelin maturation. In FGF-2-treated AMV, the number of promyelinating oligodendrocytes increased by 87% compared to saline-injected controls. The numbers of myelinating oligodendrocytes and myelin sheaths were not decreased, but conspicuous unmyelinated gaps within fibre tracts were indications of retarded myelination following FGF-2 treatment. Western blot analysis demonstrated decreased expression of CNP and a near-total loss of MOG, confirming that FGF-2 decreased myelin maturation. In contrast, IGF-I had no effect on the number of promyelinating oligodendrocytes, but increased the numbers of myelinating oligodendrocytes and myelin sheaths by 100% and 93%, respectively. Western blot analysis showed that the amount of CNP was increased following IGF-I treatment, correlating with the greater number of oligodendrocytes, but that MOG expression was lower than in controls, suggesting that the increased number of myelin sheaths in IGF-I was not matched by increased myelin maturation. The results provide in vivo evidence that FGF-2 and IGF-I control the numbers of oligodendrocytes in the brain and, respectively, retard and promote myelination.

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Localization of insulin-like growth factor-1 mRNA in murine central nervous system during postnatal development

Cited by 138 publications

References 40 publications

Light stimuli control neuronal migration by altering of insulin-like growth factor 1 (IGF-1) signaling

Light stimuli control neuronal migration by altering of insulin-like growth factor 1 (IGF-1) signaling

Insulin-like growth factor 1 regulates developing brain glucose metabolism

In vivo actions of fibroblast growth factor-2 and insulin-like growth factor-I on oligodendrocyte development and myelination in the central nervous system

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