Nogo‐B is the major form of Nogo at the floor plate and likely mediates crossing of commissural axons in the mouse spinal cord

Wang, Liqing; Yu, Chao; Wang, Jun; Leung, Pui-lam; Ma, Ding; Zhao, Hui; Taylor, Joanne; Chan, Sun On

doi:10.1002/cne.24246

Cited by 9 publications

(10 citation statements)

References 43 publications

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“…1 ). Thus, we first confirmed the previously described role of Nogo-NgR1 interactions in commissural axon guidance in the mouse spinal cord in vitro ( L. Wang et al, 2017 ), using live imaging in the embryonic chicken spinal cord ( Fig. 2 ).…”

Section: Resultssupporting

confidence: 86%

“…2 ). We incubated intact spinal cords dissected from HH22 chicken embryos in the presence of the antagonist peptide NEP1-40 for 24 h. NEP1-40 is known to inhibit the interaction of Nogo and NgR1 ( GrandPré et al, 2002 ) and was previously used to demonstrate a role of NogoB in commissural axon guidance in the embryonic mouse spinal cord in vitro ( L. Wang et al, 2017 ). In order to visualize live axon navigation, spinal cords were injected and electroporated with Math1::tdTomato-F at E3 to label dI1 neurons ( Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Whereas the role of NgR1 has been well studied in the adult brain and spinal cord, information on NgR1 and its paralogs during development of neural circuits is sparse. In mouse spinal cords cultured in the presence of NEP1-40, a Nogo-66 receptor antagonist, a role of the Nogo/NgR1 pathway for commissural axon pathfinding was suggested ( L. Wang et al, 2017 ).…”

Section: Introductionmentioning

confidence: 99%

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The Nogo-66 Receptors NgR1 and NgR3 Are Required for Commissural Axon Pathfinding

Vaccaro

Dumoulin²,

Zuñiga³

et al. 2022

J. Neurosci.

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Nogo-66 receptors (NgR1-3) are glycosylphosphatidyl inositol-linked proteins that belong to the leucine-rich repeat superfamily. Through binding to myelin-associated inhibitors, NgRs contribute to the inhibition of axonal regeneration after spinal cord injury. Their role in limiting synaptic plasticity and axonal outgrowth in the adult CNS has been described previously, but not much is known about their role during the development of the nervous system. Here, we show that NgR1 and NgR3 mRNAs are expressed during spinal cord development of the chicken embryo. In particular, they are expressed in the dI1 subpopulation of commissural neurons during the time when their axons navigate toward and across the floorplate, the ventral midline of the spinal cord. To assess a potential role of NgR1 and NgR3 in axon guidance, we downregulated them using in ovo RNAi and analyzed the trajectory of commissural axons by tracing them in open-book preparations of spinal cords. Our results show that loss of either NgR1 or NgR3 causes axons to stall in the midline area and to interfere with the rostral turn of postcrossing axons. In addition, we also show that NgR1, but not NgR3, requires neuronal PlexinA2 for the regulation of commissural axon guidance. SIGNIFICANCE STATEMENT Over the last decades, many studies have focused on the role of NgRs, particularly NgR1, in axonal regeneration in the injured adult CNS. Here, we show a physiological role of NgRs in guiding commissural axons during early development of the chicken spinal cord in vivo . Both NgR1 and NgR3 are required for midline crossing and subsequent turning of postcrossing axons into the longitudinal axis of the spinal cord. NgR1, but not NgR3, forms a receptor complex with PlexinA2 during axon guidance. Overall, these findings provide a link between neural regenerative mechanisms and developmental processes.

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Section: Resultssupporting

confidence: 86%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

The Nogo-66 Receptors NgR1 and NgR3 Are Required for Commissural Axon Pathfinding

Vaccaro

Dumoulin²,

Zuñiga³

et al. 2022

J. Neurosci.

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“…It is important to note that the developmental time point when myelin becomes abundant is much later than the appearance of nascent axon growth cones; thus, it is unlikely that MAIs play a major role in shaping neuronal networks (McKerracher and Rosen, 2015). Nonetheless, there are numerous studies examining the impact of several inhibitory molecules, especially the semaphorins, on various neurodevelopmental events (Iketani et al, 2016;Wang L. et al, 2017), but these are outside the scope of this review.…”

Section: Oligodendrocyte-axonal Growth Cone Interactionsmentioning

confidence: 99%

Glial Cell-Axonal Growth Cone Interactions in Neurodevelopment and Regeneration

2020

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The developing nervous system is a complex yet organized system of neurons, glial support cells, and extracellular matrix that arranges into an elegant, highly structured network. The extracellular and intracellular events that guide axons to their target locations have been well characterized in many regions of the developing nervous system. However, despite extensive work, we have a poor understanding of how axonal growth cones interact with surrounding glial cells to regulate network assembly. Gliato-growth cone communication is either direct through cellular contacts or indirect through modulation of the local microenvironment via the secretion of factors or signaling molecules. Microglia, oligodendrocytes, astrocytes, Schwann cells, neural progenitor cells, and olfactory ensheathing cells have all been demonstrated to directly impact axon growth and guidance. Expanding our understanding of how different glial cell types directly interact with growing axons throughout neurodevelopment will inform basic and clinical neuroscientists. For example, identifying the key cellular players beyond the axonal growth cone itself may provide translational clues to develop therapeutic interventions to modulate neuron growth during development or regeneration following injury. This review will provide an overview of the current knowledge about glial involvement in development of the nervous system, specifically focusing on how glia directly interact with growing and maturing axons to influence neuronal connectivity. This focus will be applied to the clinically-relevant field of regeneration following spinal cord injury, highlighting how a better understanding of the roles of glia in neurodevelopment can inform strategies to improve axon regeneration after injury.

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“…The co‐localization studies above supported our hypothesis that Shh may have the ability to affect the growth of neurites from POA GnRH neurons. To test this hypothesis a 3‐dimensional (3D) collagen gel assay (Rosoff et al, 2004), which has been used previously by our group and others (Fiorini and Jasoni, 2010; Low et al, 2012; Piper et al, 2009; Rosoff et al, 2004; Wang et al, 2017), was employed. GD15.5 POA explants were used, because this is the developmental time when the largest proportion of GnRH neurons are actively extending their neurites, and when GnRH neurons express Smo (Fig.…”

Section: Resultsmentioning

confidence: 99%

Developing neurites from mouse basal forebrain gonadotropin‐releasing hormone neurons use Sonic hedgehog to modulate their growth

Tan

Sheard

Jasoni

2018

Intl J of Devlp Neuroscience

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Hypothalamic gonadotropin-releasing hormone (GnRH) neurons are required for fertility in all mammalian species studied to date. GnRH neuron cell bodies reside in the basal forebrain, and most extend long neurites in the caudal direction to terminate at the median eminence (ME), the site of hormone secretion. Using in vitro neurite growth assays, histological methods, and genetic deletion strategies in mice we have analysed the role of the morphogen and neurite growth and guidance molecule, Sonic hedgehog (Shh), in the growth of GnRH neurites to their target. Immunohistochemistry revealed that Shh was present in the basal forebrain, the preoptic area (POA) and mediobasal hypothalamus (MBH) at gestational day 14.5 (GD 14.5), a time when GnRH neurites grow towards the ME. Furthermore, in situ hybridization revealed that mRNA encoding the Shh receptor, Smoothened (Smo), was present in GnRH neurons from GD 15.5, when the first GnRH neurites are extending towards the MBH. In vitro neurite growth assays using hypothalamic explants from GD 15.5 fetuses in 3-D collagen gels showed that Shh was able to significantly stimulate GnRH neurite outgrowth. Finally, genetic deletion of Smo specifically from GnRH neurons in vivo, using Cre-loxP technology, resulted in a significant decrease in GnRH neurites innervating the ME. These experiments demonstrate that GnRH neurites use Shh for their neurite development, provide further understanding of the mechanisms by which GnRH nerve terminals arrive at their site of hormone secretion, and identify an additional hypothalamic neuronal population for which Shh/Smo signaling is developmentally important.

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Nogo‐B is the major form of Nogo at the floor plate and likely mediates crossing of commissural axons in the mouse spinal cord

Cited by 9 publications

References 43 publications

The Nogo-66 Receptors NgR1 and NgR3 Are Required for Commissural Axon Pathfinding

The Nogo-66 Receptors NgR1 and NgR3 Are Required for Commissural Axon Pathfinding

Glial Cell-Axonal Growth Cone Interactions in Neurodevelopment and Regeneration

Developing neurites from mouse basal forebrain gonadotropin‐releasing hormone neurons use Sonic hedgehog to modulate their growth

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