Origin and migration of luteinizing hormone-releasing hormone neurons in mammals

Schwanzel‐Fukuda, Marlene

doi:10.1002/(sici)1097-0029(19990101)44:1<2::aid-jemt2>3.0.co;2-4

Cited by 120 publications

(54 citation statements)

References 59 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Moreover, the finding of an effect of VEGFs on the migration of GnRH neurons opens the possibility of communication between the vascular and this neuroendocrine system. It has been reported that the appearance of olfactory axons coincides with the onset of vasculogenesis in the nasal mesenchyme and precedes the initial detection of GnRH immunoreactivity in the olfactory placode (Schwanzel-Fukuda, 1999). According to this evidence, it is possible that migratory signals directed to GnRH neurons might arise from nasal mesenchyme and from the concomitant vasculogenesis.…”

Section: Role Of Neuropilin Ligands In the Migration Of Gnrh Neuronsmentioning

confidence: 83%

Neuropilins and Their Ligands Are Important in the Migration of Gonadotropin-Releasing Hormone Neurons

Cariboni¹,

Hickok²,

Rakić³

et al. 2007

J. Neurosci.

View full text Add to dashboard Cite

Gonadotropin-releasing hormone (GnRH) neurons in the hypothalamus play an important role in reproductive function. These cells originate in the nasal compartment and migrate into the basal forebrain in association with olfactory/vomeronasal nerves in embryonic life in rodents. Here, we studied the role of neuropilins and their ligands, semaphorins, in the development of the olfactory-GnRH system. We focused on Neuropilin-2 knock-out (Npn-2 ؊/؊ ) mice, because they are known to display defasciculation of olfactory nerves and reduced fertility. We found a significant decrease in the number of GnRH neurons in the hypothalamus and a marked reduction in their gonadal size. We then observed an abnormal increase of GnRH neurons in the noses of Npn-2 ؊/؊ mice, indicating that these cells failed to migrate into the forebrain. However, because neuropilins and semaphorins are involved in events of neuronal migration in the brain, we asked whether the observed reduction in GnRH neurons was directly attributable to the action of these molecules. Using fluorescenceactivated cell sorting and reverse transcription-PCR on mRNA derived from embryonic green fluorescent protein (GFP)-GnRH transgenic mice, we found expression of class 3 semaphorins and their receptors (neuropilin-1/2 and plexin-A1) in GnRH neurons. Furthermore, double-immunofluorescence experiments showed that migrating GnRH neurons, as well as associated olfactory fibers, express Npn-2 in the nasal region. We then used a line of immortalized GnRH neurons (GN11 cells) that display the same expression patterns for semaphorins and their receptors as GFP-GnRH cells and found that class 3 semaphorins and vascular endothelial growth factors modulate their migratory activity. These studies provide support for the direct involvement of neuropilins and their ligands in the establishment of the GnRH neuroendocrine system.

show abstract

Section: Role Of Neuropilin Ligands In the Migration Of Gnrh Neuronsmentioning

confidence: 83%

Neuropilins and Their Ligands Are Important in the Migration of Gonadotropin-Releasing Hormone Neurons

Cariboni¹,

Hickok²,

Rakić³

et al. 2007

J. Neurosci.

View full text Add to dashboard Cite

show abstract

“…The first port of investigation must be the GnRH neurone itself. As this neural phenotype originates outside the brain and migrates, in early embryonic life, from the developing olfactory placode into the hypothalamus (Schwanzel-Fucuda 1999), it is possible that prenatal androgens disrupt some aspect of the migratory pathway. However, despite early embryonic androgen exposure, it appears that GnRH neurones are not substantially perturbed on their migratory trek, but colonise the hypothalamus/preoptic area in similar numbers and locations to control animals in the sheep (Wood et al 1992), rat (Wray & Hoffman 1986) and rhesus monkey (Goldsmith & Song 1987).…”

Section: Gnrh Neurones and Sexual Dimorphism In Their Distributionmentioning

confidence: 99%

Prenatal programming of the female reproductive neuroendocrine system by androgens

Robinson

2006

Reproduction

View full text Add to dashboard Cite

It has been clear for several decades that the areas of the brain that control reproductive function are sexually dimorphic and that the 'programming actions' of the male gonadal steroids are responsible for sex-specific release of the gonadotrophins from the pituitary gland. The administration of exogenous steroids to fetal/neonatal animals has pinpointed windows of time in an animals' development when the reproductive neuroendocrine axis is responsive to the organisational influences of androgens. These 'critical' periods for sexual differentiation of the brain are trait-and species-specific. The neural network regulating the activity of the gonadotrophin releasing hormone (GnRH) neurones is vital to the control of reproductive function. It appears that early exposure to androgens does not influence the migratory pathway of the GnRH neurone from the olfactory placode or the size of the population of neurones that colonise the postnatal hypothalamus. However, androgens do influence the number and the nature of connections that these neurones make with other neural phenotypes. Gonadal steroid hormones play key roles in the regulation of GnRH release acting largely via steroid-sensitive intermediary neurones that impinge on the GnRH cells. Certain populations of hormonally responsive neurones have been identified that are sexually dimorphic and project from hypothalamic areas known to be involved in the regulation of GnRH release. These neurones are excellent candidates for the programming actions of male hormones in the reproductive neuroendocrine axis of the developing female.

show abstract

“…The KAL1 gene encodes anosmin-1, a neural cell adhesion molecule that modulates the migration of neuroendocrine GnRH cells from the olfactory epithelium to the hypothalamus during foetal development [6,7]. Consequently, hypogonadism in KS is due to GnRH deficiency, which most probably results from a failure of this embryonic neuronal migration [8.…”

Section: Discussionmentioning

confidence: 99%

Multiplex ligation dependent probe amplification analysis of KAL1, GNRH1, GNRHR, PROK2 and PROKR2 in male patients with idiopathic hypogonadotropic hypogonadism

Başaran¹,

Bolu²,

Ünal³

et al. 2013

Endokrynologia Polska

View full text Add to dashboard Cite

Origin and migration of luteinizing hormone-releasing hormone neurons in mammals

Cited by 120 publications

References 59 publications

Neuropilins and Their Ligands Are Important in the Migration of Gonadotropin-Releasing Hormone Neurons

Neuropilins and Their Ligands Are Important in the Migration of Gonadotropin-Releasing Hormone Neurons

Prenatal programming of the female reproductive neuroendocrine system by androgens

Multiplex ligation dependent probe amplification analysis of KAL1, GNRH1, GNRHR, PROK2 and PROKR2 in male patients with idiopathic hypogonadotropic hypogonadism

Contact Info

Product

Resources

About