Autonomous turning of cerebellar granule cells in vitro by intrinsic programs

Kumada, Tatsuro; Jiang, Yulan; Kawanami, Aya; Cameron, D. Bryant; Komuro, Hitoshi

doi:10.1016/j.ydbio.2008.11.012

Cited by 17 publications

(36 citation statements)

References 64 publications

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“…At the middle and bottom of the EGL, granule cells had a horizontally oriented soma with two horizontally extending processes (a leading process and a trailing process) ( Fig. 1 A and B) (13,14). To monitor granule cell migration in the EGL, a small amount of 1,1′-dioctadecyl-3,3,3′,3′ tetramethylindocarbocyanine perchlorate (DiI) solution was injected into the EGL of lobules V, VI, and VII of the cerebellum (Fig.…”

Section: Speed Of Granule Cell Migration In Vivo Depends On Light-darkmentioning

confidence: 99%

“…During the last 2 decades, real-time observation of cell movement demonstrated that granule cells display a distinct mode, tempo, and rate of migration as they traverse different cortical layers (13)(14)(15)(16)(17). It became apparent that granule cell migration is controlled by the orchestrated activity of multiple molecular events at the right time and right place, including pathway selection, activation of specific receptors and channels, and assembly and disassembly of cytoskeletal components (18)(19)(20)(21)(22).…”

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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: Speed Of Granule Cell Migration In Vivo Depends On Light-darkmentioning

confidence: 99%

mentioning

confidence: 99%

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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“…Although it is known that the appearance of granule cells using Golgi-staining is sporadic (Ono et al, 1997; Kumada et al, 2009), we assumed that the frequency of Golgi-stained granule cells with a particular morphological feature among the total Golgi-stained granule cells reflected the proportion of granule cells with the same morphology in the early postnatal mouse cerebella. We also assumed that the application of ethanol does not affect the efficiency of the Golgi-staining.…”

Section: Methodsmentioning

confidence: 99%

“…To attain their proper position, neurons are required to change their direction of movement at the right time and place during the journey towards their destination (Ramón y Cajal, 1929; Rakic, 1990; Yacubova and Komuro, 2003; Britanova et al, 2006; Kawauchi et al, 2006; Tanaka et al, 2006; Kumada et al, 2007; Nakajima, 2007; Cameron et al, 2007, 2009a; Kumada et at, 2009; Komuro et al, 2010). For example, in the developing cerebellum, postmitotic granule cells first migrate tangentially at the middle of the external granular layer (EGL) for 20–30 hours (Komuro et al, 2001; Komuro and Yacubova, 2003).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of cerebellar granule cell turning by alcohol

et al. 2010

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Ectopic neurons are often found in the brains of fetal alcohol spectrum disorders (FASD) and fetal alcohol syndrome (FAS) patients, suggesting that alcohol exposure impairs neuronal cell migration. Although it has been reported that alcohol decreases the speed of neuronal cell migration, little is known about whether alcohol also affects the turning of neurons. Here we show that ethanol exposure inhibits the turning of cerebellar granule cells in vivo and in vitro. First, in vivo studies using P10 mice demonstrated that a single i.p. injection of ethanol not only reduces the number of turning granule cells but also alters the mode of turning at the EGL-ML border of the cerebellum. Second, in vitro analysis using microexplant cultures of P0-P3 mouse cerebella revealed that ethanol directly reduces the frequency of spontaneous granule cell turning in a dosedependent manner. Third, the action of ethanol on the frequency of granule cell turning was significantly ameliorated by stimulating Ca 2+ and cGMP signaling or by inhibiting cAMP signaling. Taken together, these results indicate that ethanol affects the frequency and mode of cerebellar granule cell turning through alteration of the Ca 2+ and cyclic nucleotide signaling pathways, suggesting that the abnormal allocation of neurons found in the brains of FASD and FSA patients results, at least in part, from impaired turning of immature neurons by alcohol.

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“…Kumada et al [59] reported that the autonomous turning of cerebellar granule cells, that can be observed in vitro, is dependent on both calcium influx (through voltage dependent and NMDA channels) and release from intracellular stores: stimulating the release through ryanodine receptors with caffeine (1 mM) or the IP3 receptors with the agonist thimerosal (5 µM) strongly increased the frequency of turning events.…”

Section: Calcium Release From Intracellular Storesmentioning

confidence: 99%

Calcium Signaling in Neuronal Motility: Pharmacological Tools for Investigating Specific Pathways

Lovisolo

Ariano²,

Distasi³

2012

CMC

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Migration of neurons and neuronal precursors from the site of origin to their final location is a key process in the development of the nervous system and in the correct organization of neuronal structures and circuits. Different modes of migration (mainly radial and tangential) have been described in the last 40 years; for these, as for motility processes involving other cellular types, calcium signalling plays a key role, with influx from the extracellular medium representing the main mechanism, and a more delimited but specific role played by release from intracellular stores.Deciphering the involvement of the different calcium influx pathways has been a major task for cellular neurobiologists, and the availability -or lack -of reliable and selective pharmacological tools has represented the main limiting factor. This review addresses the strategies employed to investigate the role of voltage-dependent calcium channels and of neurotransmitter activated channels, either calcium permeable or not, that directly or indirectly can elicit cytosolic calcium increases; in addition, reference to recent findings on the involvement of other families of calcium permeable channels (such as the transient receptor potential superfamily) is presented. Finally, a brief description of the present -and limited -knowledge of the perturbations of calcium signalling involved in neuronal migration pathologies is provided.

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Autonomous turning of cerebellar granule cells in vitro by intrinsic programs

Cited by 17 publications

References 64 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

Inhibition of cerebellar granule cell turning by alcohol

Calcium Signaling in Neuronal Motility: Pharmacological Tools for Investigating Specific Pathways

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