Ectopic expression of luteinizing hormone-releasing hormone and peripherin in the respiratory epithelium of mice lacking transcription factor AP-2α

Kramer, Phillip R.; Guerrero, Giovanna; Krishnamurthy, Ramachandran; Mitchell, Pamela J.; Wray, Susan

doi:10.1016/s0925-4773(00)00316-6

Cited by 37 publications

(30 citation statements)

References 71 publications

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“…Tissue ablation of portions of ectoderm of the developing nose in chick and analysis of mice lacking AP-2α, which delineates presumptive respiratory epithelia from olfactory epithelia [73], suggested that GnRH-1 neurons might originate from an area of the olfactory pit that included the ectoderm responsible for the formation of the respiratory epithelium [72] (Figure 4C). Although ablation experiments (Fig.…”

Section: Embryonic Development Of Gnrh Neuronsmentioning

confidence: 99%

GnRH, anosmia and hypogonadotropic hypogonadism – Where are we?

Forni

Wray

2015

Frontiers in Neuroendocrinology

103

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Gonadotropin releasing hormone (GnRH) neurons originate the nasal placode and migrate into the brain during prenatal development. Once within the brain, these cells become integral components of the hypothalamic-pituitary-gonadal axis, essential for reproductive function. Disruption of this system causes hypogonadotropic hypogonadism (HH). HH associated with anosmia is clinically defined as Kallman syndrome (KS). Recent work examining the developing nasal region has shed new light on cellular composition, cell interactions and molecular cues responsible for the development of this system in different species. This review discusses some developmental aspects, animal models and current advancements in our understanding of pathologies affecting GnRH. In addition we discuss how development of neural crest derivatives such as the glia of the olfactory system and craniofacial structures control GnRH development and reproductive function.

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Section: Embryonic Development Of Gnrh Neuronsmentioning

confidence: 99%

GnRH, anosmia and hypogonadotropic hypogonadism – Where are we?

Forni

Wray

2015

Frontiers in Neuroendocrinology

103

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“…The work of Wray and colleagues has localized the transcription factor AP-2 to a sub-population of GnRHcontaining cells in the ventral forebrain of the developing mouse (Kramer et al, 2000a). This suggests that there may be both neural crest-derived (AP-2 positive) and adenohypophyseal-derived (AP-2 negative) GnRH cells in the ventral forebrain.…”

Section: Neural Crest Origin For Other Cell Types Associated With Thementioning

confidence: 99%

Development of the nervus terminalis: Origin and migration

Whitlock

2004

Microscopy Res & Technique

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The origin of the nervus terminalis is one of the least well understood developmental events involved in generating the cranial ganglia of the forebrain in vertebrate animals. This cranial nerve forms at the formidable interface of the anteriormost limits of migrating cranial neural crest cells, the terminal end of the neural tube and the differentiating olfactory and adenohypophyseal placodes. The complex cellular interactions that give rise to the various structures associated with the sensory placode (olfactory) and endocrine placode (adenohypophysis) surround and engulf this enigmatic cranial nerve. The tortured history of nervus terminalis development (see von Bartheld, this issue, pages 13-24) reflects the lack of consensus on the origin (or origins), as well as the experimental difficulties in uncovering the origin, of the nervus terminalis. Recent technical advances have allowed us to make headway in understanding the origin(s) of this nerve. The emergence of the externally fertilized zebrafish embryo as a model system for developmental biology and genetics has shed new light on this century-old problem. Coupled with new developmental models are techniques that allow us to trace lineage, visualize gene expression, and genetically ablate cells, adding to our experimental tools with which to follow up on studies provided by our scientific predecessors. Through these techniques, a picture is emerging in which the origin of at least a subset of the nervus terminalis cells lies in the cranial neural crest. In this review, the data surrounding this finding will be discussed in light of recent findings on neural crest and placode origins.

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“…Primary antisera used were against GnRH [polyclonal SW-1, 1:3000, (Wray et al, 1988)], peripherin (1:2000, Chemicon, Temecula, CA), p75NGFR (1:5000, Chemicon), nestin (1:3000, Kramer et al, 2000b), S100 (1:3000–4000, Dako, Glostrup, DN), GAD67 (1:8000, gift from L. J. Kopin; Oertel et al, 1981; Lee et al, 2008), PSA-NCAM (1:4000, Millipore, Billerica, MA), GFAP (Glial Fibrillary Acidic Protein, 1:18, Incstar, Stillwater, MN), Sox-10 (1:400, Forni et al, 2011), neurophysin (RN2, 1:12000, Wray et al, 1988), S100 (1:1000, Dako, Glostrup, DN), and Caspase-3 (1:200, Millipore, Billerica, MA). Alexa Fluor-546 phalloidin, (1:40, Molecular Probe, Eugene, OP) was used to visualize actin filaments.…”

Section: Methodsmentioning

confidence: 99%

“…For double-immunofluorescence experiments, primary antisera were diluted as follows: GnRH (1:1000), p75NGFR (1:1500), nestin (1:3000), S100 (1:1000–4000), and GFAP (1:5). Alexa-Fluor 488 secondary antibody or with Avidin Alexa Fluor 488 (1:1000, Molecular Probes, Eugene, OR) was used to visualize the first antigen–antibody complex, followed by blocking with anti-rabbit Fab fragment (80 μg/ml, 1 h, Jackson ImmunoResearch, West Grove, PA; Kramer et al, 2000a,b), fixation (4% formalin, 20 min), and incubation with second primary antibody, which was visualized with goat anti-rabbit CY-3 (1:1200, Jackson ImmunoResearch, West Grove, PA). Controls for double staining revealed no significant cross-reactivity (data not shown).…”

Section: Methodsmentioning

confidence: 99%

P75 nerve growth factor receptors modulate development of GnRH neurons and olfactory ensheating cells

Raucci¹,

Tiong²,

Wray³

2013

Front. Neurosci.

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Temporal and spatial localization of nerve growth factor receptor (p75NGFR) in the developing olfactory system and gonadotropin-releasing hormone-1 (GnRH) system was characterized and its role analyzed using p75NGFR null mice and nasal explants. Prenatally, p75NGFR was expressed by GnRH neurons and olfactory ensheathing cells (OECs). In p75NGFR null mice, no change in the number of GnRH cells was detected as compared to wild-type. However, in null mice, a shift in the distribution of GnRH neurons was found, with a small population of GnRH cells migrating further caudally toward the median eminence. Additionally, a reduction of both GAD67 positive olfactory axons and GFAP positive OEC fibers occurred. Acute administration of a p75NGFR blocker to GnRH cells maintained in vitro increased migration rate, consistent with the change in distribution detected in p75NGFR null mice. Chronic inhibition of p75NGFR caused an attenuation of olfactory axon fasciculation and a decrease in OEC density, again mimicking the changes detected in null mice. However, a reduction in GnRH cell number was found after chronic treatment that not observed in KO animals suggesting indirect changes occur during chronic treatment in vitro and/or a compensatory mechanism occurs in vivo that prevents loss of GnRH neurons in the absence of p75NGFR.

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Ectopic expression of luteinizing hormone-releasing hormone and peripherin in the respiratory epithelium of mice lacking transcription factor AP-2α

Cited by 37 publications

References 71 publications

GnRH, anosmia and hypogonadotropic hypogonadism – Where are we?

GnRH, anosmia and hypogonadotropic hypogonadism – Where are we?

Development of the nervus terminalis: Origin and migration

P75 nerve growth factor receptors modulate development of GnRH neurons and olfactory ensheating cells

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