The glial sling is a migratory population of developing neurons

Shu, Tianzhi; Liu, Ying; Keller, Asaf; Richards, Linda J.

doi:10.1242/dev.00514

Cited by 82 publications

(76 citation statements)

References 53 publications

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“…4F), and over time more cells within this population were observed closer to the midline ( Fig. 4L; labeled with calretinin), suggesting that the population of cells may be migrating toward the midline as they do in mouse (Shu et al, 2003c). At the same developmental stage, a second Nfia-positive population was evident more dorsally in the region of the indusium griseum (Fig.…”

Section: Key Midline Structures Are Present In Developing Human Brainmentioning

confidence: 88%

“…Several markers are known to be specific for the subcallosal sling in mouse, including NeuN, Nfia, and calretinin (CR) (Shu et al, 2003c), and all three were used to examine the presence of the subcallosal sling in coronal sections of human fetal brains aged 13, 15, and 17 weeks of gestation (Fig. 4).…”

Section: Key Midline Structures Are Present In Developing Human Brainmentioning

confidence: 99%

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Imaging, anatomical, and molecular analysis of callosal formation in the developing human fetal brain

et al. 2006

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A complex set of axonal guidance mechanisms are utilized by axons to locate and innervate their targets. In the developing mouse forebrain, we previously described several midline glial populations as well as various guidance molecules that regulate the formation of the corpus callosum. Since agenesis of the corpus callosum is associated with over 50 different human congenital syndromes, we wanted to investigate whether these same mechanisms also operate during human callosal development. Here we analyze midline glial and commissural development in human fetal brains ranging from 13 to 20 weeks of gestation using both diffusion tensor magnetic resonance imaging and immunohistochemistry. Through our combined radiological and histological studies, we demonstrate the morphological development of multiple forebrain commissures/decussations, including the corpus callosum, anterior commissure, hippocampal commissure, and the optic chiasm. Histological analyses demonstrated that all the midline glial populations previously described in mouse, as well as structures analogous to the subcallosal sling and cingulate pioneering axons, that mediate callosal axon guidance in mouse, are also present during human brain development. Finally, by Northern blot analysis, we have identified that molecules involved in mouse callosal development, including Slit, Robo, Netrin1, DCC, Nfia, Emx1,, are all expressed in human fetal brain. These data suggest that similar mechanisms and molecules required for midline commissure formation operate during both mouse and human brain development. Thus, the mouse is an excellent model system for studying normal and pathological commissural formation in human brain development.

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Section: Key Midline Structures Are Present In Developing Human Brainmentioning

confidence: 88%

Section: Key Midline Structures Are Present In Developing Human Brainmentioning

confidence: 99%

Imaging, anatomical, and molecular analysis of callosal formation in the developing human fetal brain

et al. 2006

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“…Cortical commissural axons rely on cues provided by a population of cells named the "glial sling" to successfully navigate the midline. Neurons that form the glial sling derive from the SVZ and migrate toward the midline around E17.5, just before the arrival of the first commissural axons (Shu et al 2003b). In mouse mutants for one of the Nuclear factor I genes, Nfia, sling cells fail to reach the midline and instead migrate toward the septum.…”

Section: Migration Of Guidepost Cells For Axon Guidancementioning

confidence: 99%

Guiding Neuronal Cell Migrations

Marı́n¹,

Valiente²,

Ge³

et al. 2010

Cold Spring Harbor Perspectives in Biology

375

351

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Neuronal migration is, along with axon guidance, one of the fundamental mechanisms underlying the wiring of the brain. As other organs, the nervous system has acquired the ability to grow both in size and complexity by using migration as a strategy to position cell types from different origins into specific coordinates, allowing for the generation of brain circuitries. Guidance of migrating neurons shares many features with axon guidance, from the use of substrates to the specific cues regulating chemotaxis. There are, however, important differences in the cell biology of these two processes. The most evident case is nucleokinesis, which is an essential component of migration that needs to be integrated within the guidance of the cell. Perhaps more surprisingly, the cellular mechanisms underlying the response of the leading process of migrating cells to guidance cues might be different to those involved in growth cone steering, at least for some neuronal populations.

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“…8). An additional mechanism of guidance at the cortical midline occurs via transient neuronal populations that form the subcallosal sling and a cellular corridor for callosal axons to cross the midline (Shu et al, 2003b;Niquille et al, 2009). We stained sections from both KOs and WT littermates with antibodies against the transcription factor Nfia, which labels the subcallosal sling (Shu et al, 2003a) and found it to be intact in both Slc12a6…”

Section: ⌬18/⌬18mentioning

confidence: 99%

Loss of Neuronal Potassium/Chloride Cotransporter 3 (KCC3) Is Responsible for the Degenerative Phenotype in a Conditional Mouse Model of Hereditary Motor and Sensory Neuropathy Associated with Agenesis of the Corpus Callosum

Shekarabi

Moldrich²,

Rasheed³

et al. 2012

J. Neurosci.

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Disruption of the potassium/chloride cotransporter 3 (KCC3), encoded by the SLC12A6 gene, causes hereditary motor and sensory neuropathy associated with agenesis of the corpus callosum (HMSN/ACC), a neurodevelopmental and neurodegenerative disorder affecting both the peripheral nervous system and CNS. However, the precise role of KCC3 in the maintenance of ion homeostasis in the nervous system and the pathogenic mechanisms leading to HMSN/ACC remain unclear. We established two Slc12a6 Cre/LoxP transgenic mouse lines expressing C-terminal truncated KCC3 in either a neuron-specific or ubiquitous fashion. Our results suggest that neuronal KCC3 expression is crucial for axon volume control. We also demonstrate that the neuropathic features of HMSN/ACC are predominantly due to a neuronal KCC3 deficit, while the auditory impairment is due to loss of non-neuronal KCC3 expression. Furthermore, we demonstrate that KCC3 plays an essential role in inflammatory pain pathways. Finally, we observed hypoplasia of the corpus callosum in both mouse mutants and a marked decrease in axonal tracts serving the auditory cortex in only the general deletion mutant. Together, these results establish KCC3 as an important player in both central and peripheral nervous system maintenance.

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The glial sling is a migratory population of developing neurons

Cited by 82 publications

References 53 publications

Imaging, anatomical, and molecular analysis of callosal formation in the developing human fetal brain

Imaging, anatomical, and molecular analysis of callosal formation in the developing human fetal brain

Guiding Neuronal Cell Migrations

Loss of Neuronal Potassium/Chloride Cotransporter 3 (KCC3) Is Responsible for the Degenerative Phenotype in a Conditional Mouse Model of Hereditary Motor and Sensory Neuropathy Associated with Agenesis of the Corpus Callosum

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