LHRH neuronal migration: heterotypic transplantation analysis of guidance cues

Gao, Chen; Noden, Drew M.; Norgren, Robert B.

doi:10.1002/(sici)1097-4695(200001)42:1<95::aid-neu9>3.0.co;2-2

Cited by 13 publications

(7 citation statements)

References 41 publications

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“…Migratory GnRH neurons receive a plethora of guidance and movement-inducing messages during this journey, which are likely to be distinct depending on the stage of their migration (Tobet & Schwarting, 2006). Signals may act directly or indirectly through the extension of olfactory axons, as disruption of the nerve tract "scaffolds" themselves can disrupt GnRH migration (Gao et al, 2000). Gradients of chemokines may be particularly important for promoting the movement of GnRH neurons (Tobet & Schwarting, 2006).…”

Section: Discussionmentioning

confidence: 99%

IGSF 10 mutations dysregulate gonadotropin‐releasing hormone neuronal migration resulting in delayed puberty

et al. 2016

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Early or late pubertal onset affects up to 5% of adolescents and is associated with adverse health and psychosocial outcomes. Self‐limited delayed puberty (DP) segregates predominantly in an autosomal dominant pattern, but the underlying genetic background is unknown. Using exome and candidate gene sequencing, we have identified rare mutations in IGSF10 in 6 unrelated families, which resulted in intracellular retention with failure in the secretion of mutant proteins. IGSF10 mRNA was strongly expressed in embryonic nasal mesenchyme, during gonadotropin‐releasing hormone (GnRH) neuronal migration to the hypothalamus. IGSF10 knockdown caused a reduced migration of immature GnRH neurons in vitro, and perturbed migration and extension of GnRH neurons in a gnrh3:EGFP zebrafish model. Additionally, loss‐of‐function mutations in IGSF10 were identified in hypothalamic amenorrhea patients. Our evidence strongly suggests that mutations in IGSF10 cause DP in humans, and points to a common genetic basis for conditions of functional hypogonadotropic hypogonadism (HH). While dysregulation of GnRH neuronal migration is known to cause permanent HH, this is the first time that this has been demonstrated as a causal mechanism in DP.‡

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Section: Discussionmentioning

confidence: 99%

IGSF 10 mutations dysregulate gonadotropin‐releasing hormone neuronal migration resulting in delayed puberty

et al. 2016

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“…In spite of the change in developmental environment in the present study, LHRH neurons were accompanied by the ectopic olfactory fibers that express SST and axonin‐1 after they entered the spinal nerve. A recent transplantation study of the olfactory placode to the region of the trigeminal placode found that LHRH neurons migrated into the trigeminal ganglion and metencephalon in association with the ectopic olfactory nerve (Gao et al ., 2000). This is compatible with our previous findings that LHRH neurons migrate along with trigeminal nerve under normal and experimental conditions (Murakami et al ., 1991, 1995, 1998).…”

Section: Discussionmentioning

confidence: 99%

Migration of LHRH neurons into the spinal cord: evidence for axon‐dependent migration from the transplanted chick olfactory placode

Murakami

Arai

2002

Eur J of Neuroscience

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In the chick embryo, luteinizing hormone-releasing hormone (LHRH) neurons originate in the olfactory placode and migrate along the olfactory nerve to the forebrain. In previous studies, we demonstrated that LHRH neurons followed the trigeminal nerve when the olfactory nerve was physically interrupted. To examine whether LHRH neurons possess the capacity to migrate along the different type of axons, the olfactory placode was transplanted into the base of the forelimb. Three to five days after the transplantation, LHRH neurons were detectable in the spinal nerve, the dorsal root ganglion, the sympathetic ganglion and the spinal cord. Double or triple labelling studies for LHRH, somatostatin and/or axonin-1 showed that LHRH neurons entered the spinal nerve in contact with the olfactory axons, which are specifically immunoreactive to somatostatin. Migrating LHRH neurons continued to associate closely with the olfactory axons in the spinal nerve. However, some LHRH neurons often migrated along with the axonin-1 positive spinal sensory axons, maintaining a distance from the olfactory axons. Furthermore, a few LHRH neurons were observed in the ventral root and the ventral funiculus independent of olfactory axons. As LHRH neurons were observed in the motor component of the spinal nerve, it is probable that LHRH neurons also invaded the spinal cord using the motor axons as a guiding substrate for their migration. These results suggest that the migration mode of LHRH neurons is axon dependent in the peripheral region, however, chemical identity with regard to axonal substrate choice for migration was not specified in the present study.

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“…An important relationship exists between olfactory axons and GnRH neurons. In mice, if olfactory axons do not cross the cribriform plate or do not reach proper brain targets, GnRH neurons remain in the nose or are found in aberrant locations respectively (Murakami and Arai, 1994;Deiner and Sretavan, 1999;Rugarli, 1999;Gao et al, 2000;MacColl et al, 2002). In patients with Kallmann syndrome, malformation of the olfactory system and failure of GnRH neurons to migrate into the brain results in anosmia and delayed or absent pubertal maturation (hypogonadotropic hypogonadism) (Iovane et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

SDF and GABA interact to regulate axophilic migration of GnRH neurons

Casoni

Hutchins

Donohue

et al. 2012

Journal of Cell Science

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SummaryStromal derived growth factor (SDF-1) and gamma-aminobutyric acid (GABA) are two extracellular cues that regulate the rate of neuronal migration during development and may act synergistically. The molecular mechanisms of this interaction are still unclear. Gonadotropin releasing hormone-1 (GnRH) neurons are essential for vertebrate reproduction. During development, these neurons emerge from the nasal placode and migrate through the cribriform plate into the brain. Both SDF-1 and GABA have been shown to regulate the rate of GnRH neuronal migration by accelerating and slowing migration, respectively. As such, this system was used to explore the mechanism by which these molecules act to produce coordinated cell movement during development. In the present study, GABA and SDF-1 are shown to exert opposite effects on the speed of cell movement by activating depolarizing or hyperpolarizing signaling pathways, GABA via changes in chloride and SDF-1 via changes in potassium. GABA and SDF-1 were also found to act synergistically to promote linear rather than random movement. The simultaneous activation of these signaling pathways, therefore, results in tight control of cellular speed and improved directionality along the migratory pathway of GnRH neurons.

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LHRH neuronal migration: heterotypic transplantation analysis of guidance cues

Cited by 13 publications

References 41 publications

IGSF 10 mutations dysregulate gonadotropin‐releasing hormone neuronal migration resulting in delayed puberty

IGSF 10 mutations dysregulate gonadotropin‐releasing hormone neuronal migration resulting in delayed puberty

Migration of LHRH neurons into the spinal cord: evidence for axon‐dependent migration from the transplanted chick olfactory placode

SDF and GABA interact to regulate axophilic migration of GnRH neurons

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