Axonal pathfinding mechanisms at the cortical midline and in the development of the corpus callosum

Lj, Richards

doi:10.1590/s0100-879x2002001200004

Cited by 41 publications

(30 citation statements)

References 69 publications

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“…The levels of fibronectin and laminin-1 present in astrocyte-conditioned medium were normalized for biglycan, a proteoglycan whose release by astrocytes is not affected by carbachol treatment. 4 It should be noticed that fibronectin levels were considerably higher than those of laminin, in agreement with a previous report (61).…”

Section: Resultssupporting

confidence: 91%

Modulation of Neuritogenesis by Astrocyte Muscarinic Receptors

Guizzetti

Moore

Giordano

et al. 2008

Journal of Biological Chemistry

125

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Astrocytes have been shown to release factors that have promoting or inhibiting effects on neuronal development. However, mechanisms controlling the release of such factors from astrocytes are not well established. Astrocytes express muscarinic receptors whose activation stimulates a robust intracellular signaling, although the role of these receptors in glial cells is not well understood. Acetylcholine and acetylcholine receptors are present in the brain before synaptogenesis occurs and are believed to be involved in neuronal maturation. The present study was undertaken to investigate whether stimulation of muscarinic receptors in astrocytes would modulate neurite outgrowth in hippocampal neurons. Rat hippocampal neurons, cocultured with rat cortical astrocytes previously exposed to the cholinergic agonist carbachol, displayed longer neurites. The effect of carbachol in astrocytes was due to the activation of M3 muscarinic receptors. Exposure of astrocytes to carbachol increased the expression of the extracellular matrix proteins fibronectin and laminin-1 in these cells. This effect was mediated in part by an increase in laminin-1 and fibronectin mRNA levels and in part by the up-regulation of the production and release of plasminogen activator inhibitor-1, an inhibitor of the proteolytic degradation of the extracellular matrix. The inhibition of fibronectin activity strongly reduced the effect of carbachol on the elongation of all the neurites, whereas inhibition of laminin-1 activity reduced the elongation of minor neurites only. Plasminogen activator inhibitor-1 also induced neurite elongation through a direct effect on neurons. Taken together, these results demonstrate that cholinergic muscarinic stimulation of astrocytes induces the release of permissive factors that accelerate neuronal development.

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Section: Resultssupporting

confidence: 91%

Modulation of Neuritogenesis by Astrocyte Muscarinic Receptors

Guizzetti

Moore

Giordano

et al. 2008

Journal of Biological Chemistry

125

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“…Knockout studies in mice have demonstrated the involvement of a number of different genes in callosal development (reviewed in Richards, 2002;Richards et al, 2004b). These genes include guidance factors such as Slit2 (Bagri et al, 2002) and Netrin1 (Serafini et al, 1996), receptor molecules such as Robo (Richards et al, 2004a), DCC (Fazeli et al, 1997), and Npn1 (Gu et al, 2003), transcription factors such as Nfia (Shu et al, 2003b), Emx1 (Qiu et al, 1996;Yoshida et al, 1997), and Emx-2 (Pellegrini et al, 1996;Yoshida et al, 1997;Martins et al, 2004), as well as GAP43 (Shen et al, 2002).…”

Section: Expression Of Commissural Regulatory Genes In Developing Hummentioning

confidence: 99%

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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“…More dorsally, midline glial populations that make up the 'glial sling', 'glial wedge', and indusium griseum have all been implicated in midline crossing in the corpus callosum (Richards, 2002a;Shu et al, 2003a;Shu et al, 2003b;Shu et al, 2003c;Shu and Richards, 2001;Silver et al, 1982;Silver and Ogawa, 1983). Little is known about how midline cells influence the formation of the forebrain commissures.…”

Section: Introductionmentioning

confidence: 99%

Hedgehog regulated Slit expression determines commissure and glial cell position in the zebrafish forebrain

et al. 2005

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Three major axon pathways cross the midline of the vertebrate forebrain early in embryonic development: the postoptic commissure (POC), the anterior commissure (AC) and the optic nerve. We show that a small population of Gfap+astroglia spans the midline of the zebrafish forebrain in the position of, and prior to, commissural and retinal axon crossing. These glial `bridges' form in regions devoid of the guidance molecules slit2 and slit3,although a subset of these glial cells express slit1a. We show that Hh signaling is required for commissure formation, glial bridge formation, and the restricted expression of the guidance molecules slit1a, slit2, slit3 and sema3d, but that Hh does not appear to play a direct role in commissural and retinal axon guidance. Reducing Slit2 and/or Slit3 function expanded the glial bridges and caused defasciculation of the POC, consistent with a `channeling' role for these repellent molecules. By contrast, reducing Slit1a function led to reduced midline axon crossing, suggesting a distinct role for Slit1a in midline axon guidance. Blocking Slit2 and Slit3, but not Slit1a, function in the Hh pathway mutant yot (gli2DR) dramatically rescued POC axon crossing and glial bridge formation at the midline, indicating that expanded Slit2 and Slit3 repellent function is largely responsible for the lack of midline crossing in these mutants. This analysis shows that Hh signaling helps to pattern the expression of Slit guidance molecules that then help to regulate glial cell position and axon guidance across the midline of the forebrain.

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Axonal pathfinding mechanisms at the cortical midline and in the development of the corpus callosum

Cited by 41 publications

References 69 publications

Modulation of Neuritogenesis by Astrocyte Muscarinic Receptors

Modulation of Neuritogenesis by Astrocyte Muscarinic Receptors

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

Hedgehog regulated Slit expression determines commissure and glial cell position in the zebrafish forebrain

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