Neural Crest and Ectodermal Cells Intermix in the Nasal Placode to Give Rise to GnRH-1 Neurons, Sensory Neurons, and Olfactory Ensheathing Cells

Forni, Paolo E.; Taylor-Burds, Carol; Melvin, Vida Senkus; Williams, Taylor; Wray, Susan

doi:10.1523/jneurosci.6087-10.2011

Cited by 188 publications

(253 citation statements)

References 104 publications

(136 reference statements)

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“…These results imply that GnRH3 neurons may arise from neural crest cells, most likely those in the medial migratory pathway. This idea is in good agreement with recent cell fatemapping studies in chicks and mice, indicating that neural crest cells give rise to a subpopulation of GnRH1 neurons and olfactory ensheathing glial cells (Barraud et al, 2010;Forni et al, 2011). Since sox10 expression is maintained in the medial migration pathway and not on the lateral pathway, it is tempting to speculate that GnRH3 neurons may be derived from sox10 mRNA-expressing neural crest cells in the medial migration pathway, while GnRH2 neurons are derived from other populations of neural crest cells.…”

Section: Discussionsupporting

confidence: 90%

Regulation of Temporal and Spatial Organization of Newborn GnRH Neurons by IGF Signaling in Zebrafish

Onuma¹,

Ding²,

Abraham³

et al. 2011

J. Neurosci.

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When and how newborn neurons are organized to form a functional network in the developing brain remains poorly understood. An attractive model is the gonadotropin-releasing hormone (GnRH) neuron system, master regulator of the reproductive axis. Here we show that blockage of IGF signaling, a central growth-promoting signaling pathway, by the induced expression of a dominant-negative form of IGF1 receptor (IGF1R) or specific IGF1R inhibitors delayed the emergence of GnRH2 neurons in the midbrain and GnRH3 neurons in the olfactory bulb region. Blockage of IGF signaling also resulted in an abnormal appearance of GnRH3 neurons outside of the olfactory bulb region, although it did not change the locations of other olfactory neurons, GnRH2 neurons, or brain patterning. This IGF action is developmental stage-dependent because the blockade of IGF signaling in advanced embryos had no such effect. An application of phosphatidylinositol 3-kinase (PI3K) inhibitors phenocopied the IGF signaling deficient embryos, whereas the MAPK inhibitors had no effect, suggesting that this IGF action is mediated through the PI3K pathway. Real-time in vivo imaging studies revealed that the ectopic GnRH3 neurons emerged at the same time as the normal GnRH3 neurons in IGF-deficient embryos. Further experiments suggest that IGF signaling affects the spatial distribution of newborn GnRH3 neurons by influencing neural crest cell migration and/or differentiation. These results suggest that the IGF-IGF1R-PI3K pathway regulates the precise temporal and spatial organization of GnRH neurons in zebrafish and provides new insights into the regulation of GnRH neuron development.

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Section: Discussionsupporting

confidence: 90%

Regulation of Temporal and Spatial Organization of Newborn GnRH Neurons by IGF Signaling in Zebrafish

Onuma¹,

Ding²,

Abraham³

et al. 2011

J. Neurosci.

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“…Contribution of NCCs to other sensory organs is still being investigated. Only recently has it been shown by lineage tracing that glial ensheathing cells and subpopulations of neurons in the 5411 RESEARCH ARTICLE Dual origin of the otic vesicle olfactory system originate from NCCs that were fate mapped using Wnt1-Cre (Barraud et al, 2010;Forni et al, 2011). We also observed Wnt1-Cre and Pax3…”

Section: Dual Origin Of the Ov And Cvgmentioning

confidence: 77%

Dual embryonic origin of the mammalian otic vesicle forming the inner ear

2011

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SUMMARYThe inner ear and cochleovestibular ganglion (CVG) derive from a specialized region of head ectoderm termed the otic placode. During embryogenesis, the otic placode invaginates into the head to form the otic vesicle (OV), the primordium of the inner ear and CVG. Non-autonomous cell signaling from the hindbrain to the OV is required for inner ear morphogenesis and neurogenesis. In this study, we show that neuroepithelial cells (NECs), including neural crest cells (NCCs), can contribute directly to the OV from the neural tube. Using Wnt1-Cre, Pax3Cre/+ and Hoxb1 Cre/+ mice to label and fate map cranial NEC lineages, we have demonstrated that cells from the neural tube incorporate into the otic epithelium after otic placode induction has occurred. Pax3Cre/+ labeled a more extensive population of NEC derivatives in the OV than did Wnt1-Cre. NEC derivatives constitute a significant population of the OV and, moreover, are regionalized specifically to proneurosensory domains. Descendents of Pax3 Cre/+ and Wnt1-Cre labeled cells are localized within sensory epithelia of the saccule, utricle and cochlea throughout development and into adulthood, where they differentiate into hair cells and supporting cells. Some NEC derivatives give rise to neuroblasts in the OV and CVG, in addition to their known contribution to glial cells. This study defines a dual cellular origin of the inner ear from sensory placode ectoderm and NECs, and changes the current paradigm of inner ear neurosensory development.

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“…Data from the past few years suggest that GnRH neurons originate from both the neural crest and ectodermal progenitors, and migrate in close association with growing axons of olfactory and/or terminal nerves. 15,16 Once in the hypothalamus, GnRH neurons detach from their axonal guides, disperse further into the brain parenchyma and stop migrating. At birth, GnRH neurons have reached their final destination in the brain and many of them project into the median eminence, where they release the GnRH decapeptide from their axon terminals into the hypophyseal portal vasculature.…”

Section: Biology Of the Gnrh Neuronal Systemmentioning

confidence: 99%

European Consensus Statement on congenital hypogonadotropic hypogonadism—pathogenesis, diagnosis and treatment

et al. 2015

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| Congenital hypogonadotropic hypogonadism (CHH) is a rare disorder caused by the deficient production, secretion or action of gonadotropin-releasing hormone (GnRH), which is the master hormone regulating the reproductive axis. CHH is clinically and genetically heterogeneous, with >25 different causal genes identified to date. Clinically, the disorder is characterized by an absence of puberty and infertility. The association of CHH with a defective sense of smell (anosmia or hyposmia), which is found in ~50% of patients with CHH is termed Kallmann syndrome and results from incomplete embryonic migration of GnRHsynthesizing neurons. CHH can be challenging to diagnose, particularly when attempting to differentiate it from constitutional delay of puberty. A timely diagnosis and treatment to induce puberty can be beneficial for sexual, bone and metabolic health, and might help minimize some of the psychological effects of CHH. In most cases, fertility can be induced using specialized treatment regimens and several predictors of outcome have been identified. Patients typically require lifelong treatment, yet ~10-20% of patients exhibit a spontaneous recovery of reproductive function. This Consensus Statement summarizes approaches for the diagnosis and treatment of CHH and discusses important unanswered questions in the field.

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Neural Crest and Ectodermal Cells Intermix in the Nasal Placode to Give Rise to GnRH-1 Neurons, Sensory Neurons, and Olfactory Ensheathing Cells

Cited by 188 publications

References 104 publications

Regulation of Temporal and Spatial Organization of Newborn GnRH Neurons by IGF Signaling in Zebrafish

Regulation of Temporal and Spatial Organization of Newborn GnRH Neurons by IGF Signaling in Zebrafish

Dual embryonic origin of the mammalian otic vesicle forming the inner ear

European Consensus Statement on congenital hypogonadotropic hypogonadism—pathogenesis, diagnosis and treatment

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