Brain-Derived Neurotrophic Factor Participates in Determination of Neuronal Laminar Fate in the Developing Mouse Cerebral Cortex

Fukumitsu, Hidefumi; Ohtsuka, Masanari; Murai, Rina; Nakamura, Hiroyuki; Itoh, Kazuyoshi; Furukawa, Shoei

doi:10.1523/jneurosci.4251-06.2006

Cited by 92 publications

(81 citation statements)

References 54 publications

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“…Neurons can, for example, signal back to progenitor cells via cardiotrophin-1 and, in doing so, instruct them to produce astrocytes instead of neurons 9 . Brain-derived neurotrophic factor (BDNF) administered in the ventricular lumen at E13.5 induces deep-layer characteristics in cells destined for layer 4, whereas an antibody to BDNF changed some of these cells to layer 2/3 type neurons, suggesting that BDNF is an extrinsic cortical cell-fate modifier 32 .…”

Section: Discussionmentioning

confidence: 99%

Sip1 regulates sequential fate decisions by feedback signaling from postmitotic neurons to progenitors

et al. 2009

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The fate of cortical progenitors, which progressively generate neurons and glial cells during development, is determined by temporally and spatially regulated signaling mechanisms. We found that the transcription factor Sip1 (Zfhx1b), which is produced at high levels in postmitotic neocortical neurons, regulates progenitor fate non-cell autonomously. Conditional deletion of Sip1 in young neurons induced premature production of upper-layer neurons at the expense of deep layers, precocious and increased generation of glial precursors, and enhanced postnatal astrocytogenesis. The premature upper-layer generation coincided with overexpression of the neurotrophin-3 (Ntf3) gene and upregulation of fibroblast growth factor 9 (Fgf9) gene expression preceded precocious gliogenesis. Exogenous application of Fgf9 to mouse cortical slices induced excessive generation of glial precursors in the germinal zone. Our data suggest that Sip1 restrains the production of signaling factors in postmitotic neurons that feed back to progenitors to regulate the timing of cell fate switch and the number of neurons and glial cells throughout corticogenesis.

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Section: Discussionmentioning

confidence: 99%

Sip1 regulates sequential fate decisions by feedback signaling from postmitotic neurons to progenitors

et al. 2009

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“…The developmental potential of forebrain cortical neuronal precursors becomes progressively restricted over time (Desai and McConnell 2000), and these cells are typically fated by signals received during a rather restricted time window around their last mitosis, within or close to the ventricular zone. Another key feature of cortical neuron development is that such fatedeWning signals can only be realized by cycling cells, and indeed cell sensitivity toward such signals varies over the cell cycle (e.g., McConnell and Kaznowski 1991;Fukumitsu et al 2006;Leone et al 2008). …”

Section: Development and Diverentiation Of Cerebellar (Cortical) Inhimentioning

confidence: 99%

Besides Purkinje cells and granule neurons: an appraisal of the cell biology of the interneurons of the cerebellar cortex

Schilling

Oberdick

Rossi

et al. 2008

Histochem Cell Biol

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Ever since the groundbreaking work of Ramon y Cajal, the cerebellar cortex has been recognized as one of the most regularly structured and wired parts of the brain formed by a rather limited set of distinct cells. Its rather protracted course of development, which persists well into postnatal life, the availability of multiple natural mutants, and, more recently, the availability of distinct molecular genetic tools to identify and manipulate discrete cell types have suggested the cerebellar cortex as an excellent model to understand the formation and working of the central nervous system. However, the formulation of a unifying model of cerebellar function has so far proven to be a most cantankerous problem, not least because our understanding of the internal cerebellar cortical circuitry is clearly spotty. Recent research has highlighted the fact that cerebellar cortical interneurons are a quite more diverse and heterogeneous class of cells than generally appreciated, and have provided novel insights into the mechanisms that underpin the development and histogenetic integration of these cells. Here, we provide a short overview of cerebellar cortical interneuron diversity, and we summarize some recent results that are hoped to provide a primer on current understanding of cerebellar biology.

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“…Alcohol exposure consisted of a range of doses to determine possible threshold levels for causing effects. The timing of alcohol exposure coincided with the first two trimesters-equivalent to human gestation (Bayer et al, 1993;Dobbing, 1981;Dobbing and Sands, 1973;1979), a period of time before and during the generation of neocortical neurons (Fukumitsu et al, 2006;Kennedy and Elliot, 1985;Miller, 1986;1987;. Morphological analyses were carried out in offspring during the time period shown previously to have transitory CC axons (Elberger 1994a,b).…”

Section: Introductionmentioning

confidence: 99%

Alcohol exposure during the first two trimesters-equivalent alters the development of corpus callosum projection neurons in the rat

Livy

Elberger

2008

Alcohol

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Children exposed prenatally to alcohol can display a variety of neural deficits, including an altered development of the corpus callosum (CC), the largest interhemispheric axon pathway in the brain. Furthermore, these children show functional abnormalities that are related to brain regions with significant numbers of CC connections. Little is known about how alcohol imparts influence on CC development, but one possible mechanism is by affecting the corpus callosum projection neurons (CCpn) directly. The purpose of this study was to quantify the effects of prenatal alcohol exposure on the number, size and distribution of CCpn within the visual cortex. The visual cortex was selected specifically due to the many vision-related deficits noted in fetal alcohol exposed children and because the critical role of the CC in visual cortex development is well documented. Sprague-Dawley rat pups received one of four alcohol dosages during gestational days (G) 1-20, or reared as nutritional or untreated control animals. Each litter was categorized according to the peak blood alcohol concentration (BAC) experienced. Pups were removed from each litter on days equivalent to G29, G36, G43, and G50, for histology and measurement. Callosal axons were labelled retrogradely to their CCpn using DiI and the CCpn were then examined using confocal laser scanning microscopy. Differences between alcohol-exposed and control animals were observed in CCpn cell body size, number, and location with the cortex. This was particularly true of animals exposed to high doses of alcohol. In addition, some trends of CCpn development were found to be unchanged as a result of prenatal alcohol exposure. The results demonstrate clear differences in the development of CCpn in the visual cortex between alcohol-exposed and control animals and suggest that this development is particularly affected in those animals exposed to high doses of alcohol.

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Brain-Derived Neurotrophic Factor Participates in Determination of Neuronal Laminar Fate in the Developing Mouse Cerebral Cortex

Cited by 92 publications

References 54 publications

Sip1 regulates sequential fate decisions by feedback signaling from postmitotic neurons to progenitors

Sip1 regulates sequential fate decisions by feedback signaling from postmitotic neurons to progenitors

Besides Purkinje cells and granule neurons: an appraisal of the cell biology of the interneurons of the cerebellar cortex

Alcohol exposure during the first two trimesters-equivalent alters the development of corpus callosum projection neurons in the rat

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