Ontogenesis of the GnRH neuron system in the rat. A quantitative immunohistochemical study with special reference to the extra cerebral GnRH-positive cells and the occupation of intracerebral termination fields

Sétáló, G.; Hagino, Nobuyoshi; Dittrich, Ernő

doi:10.1016/0143-4179(92)90520-7

Cited by 13 publications

(8 citation statements)

References 23 publications

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“…However, the increase in the number and percentage of GnRH neurons in the caudal area of the migration trajectory is generally considered as a manifestation of their continuous arrival from the nasal cranium and more rostral forebrain regions. The stabilization of the numbers of GnRH neurons in the septo-preoptic area and the hypothalamus of rats occurs by the end of foetal life, suggesting the cessation of their migration (Sétáló et al 1992). This conclusion is supported by our observation that the distribution of GnRH-ir neurons in saline-treated rats shows an increase in their proportion in the septo-preoptic area and hypothalamus between E17 and E21.…”

Section: Influence Of Cas On Gnrh Neuron Migrationmentioning

confidence: 98%

The influence of catecholamine on the migration of gonadotropin-releasing hormone-producing neurons in the rat foetuses

et al. 2008

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Catecholamines (CA) play an important role in the regulation of GnRH neurons in adults, and it is probable that they control GnRH-neuron development. Migration of GnRH neurons was evaluated in male and female rats at the 17th embryonic day (E17) and E21, following the daily treatment of their pregnant mothers from the 11th to the 16th and 20th day of gestation with alpha-methyl-para-tyrosine (alphaMPT), an inhibitor of catecholamine synthesis. High-performance liquid chromatography with electrochemical detection (HPLC-ED) was used to specify the alphaMPT-induced CA depletion. There was a 50-70% decrease in dopamine and noradrenaline content in the nose and in the brain of alphaMPT-treated foetuses, proving the efficacy of this pharmacological model. Immunohistochemistry was used to evaluate the percentage (%) of GnRH neurons along their migration pathway from the vomeronasal organ (VNO) in the nose to the septo-preoptic area in the forebrain which is considered as an index of neuron migration. Special attention was paid to the topographic relationships of GnRH neurons with catecholaminergic fibres. These were observed in apposition with GnRH neurons in the entrance to the forebrain. In CA-deficient foetuses, the percentage of GnRH neurons located in the rostral regions extending from the VNO to the septum was greater than in controls. However, no statistically significant difference was found in the forebrain which extended from the septum to the retrochiasmatic area. In conclusion, these data suggest that endogenous catecholamines stimulate the GnRH neuron migration in ontogenesis.

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Section: Influence Of Cas On Gnrh Neuron Migrationmentioning

confidence: 98%

The influence of catecholamine on the migration of gonadotropin-releasing hormone-producing neurons in the rat foetuses

et al. 2008

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“…Positioning of GnRH neurons as a continuum from the medial septum to the anterior hypothalamus in the brain is dependent on their birth order from E9.5 to 12.5 in the mice [46] and the later-generated neurons by E11.5-12.5 are found to be localized to the caudal region of the POA and the anterior hypothalamus. Therefore, the maternal DEX treatment from the E13-20 stage coincides with the GnRH neuronal development in the rat [4,10], suggesting that the later-generated GnRH neurons might have been affected by DEX exposure leading to their decreased motility observed in vitro.…”

Section: Discussionmentioning

confidence: 99%

“…Increasing numbers of GnRH-expressing neurons have been shown along the migratory route into the brain across successive embryonic and neonatal stages [9,10]. However, stabilization of GnRH neuronal number in the rat brain by late E20 stage until the day of birth [10] possibly suggests the termination of GnRH neuronal migration.…”

Section: Introductionmentioning

confidence: 99%

“…GnRH neurons migrate along the vomeronasal axons crossing the cribriform plate [5,6], which turn caudally along the vomeronasal nerve (VNN) towards the basal forebrain [7] and finally dissociate from their guiding axons to attain their position in the brain [8]. Increasing numbers of GnRH-expressing neurons have been shown along the migratory route into the brain across successive embryonic and neonatal stages [9,10]. However, stabilization of GnRH neuronal number in the rat brain by late E20 stage until the day of birth [10] possibly suggests the termination of GnRH neuronal migration.…”

Section: Introductionmentioning

confidence: 99%

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Maternal Dexamethasone Exposure Inhibits the Gonadotropin-Releasing Hormone Neuronal Movement in the Preoptic Area of Rat Offspring

Lim

Soga²,

Parhar³

2014

Dev Neurosci

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Migration and final positioning of gonadotropin-releasing hormone (GnRH) neurons in the preoptic area (POA) is critical for reproduction. It is known that maternal dexamethasone (DEX) exposure impairs reproductive function and behaviour in the offspring. However, it is still not known whether maternal DEX exposure affects the postnatal GnRH neurons in the offspring. This study determined the neuronal movement of enhanced green fluorescent protein (EGFP)-tagged GnRH neurons in slice culture of postnatal day 0 (P0), P5 and P50-60 transgenic male rats. Effect of maternal DEX treatment on EGFP-GnRH neuronal movement and F-actin distribution on GnRH neurons at P0 stage were studied. Time-lapse analysis of P0 and P5 EGFP-GnRH neurons displayed active cellular movement within the POA compared to young adult P50-60 stages, suggesting possible fine-tuning movement for positioning of early postnatal GnRH neurons. The DEX-treated EGFP-GnRH neurons demonstrated decreased motility in the POA and reduced F-actin distribution in the GnRH neurons at 60 h culture compared to the vehicle-treated. These results suggest that the P0 GnRH neuronal movement in the POA is altered by maternal DEX exposure, which possibly disrupts the fine-tuning process for positioning and development of early postnatal GnRH neurons in the brain, potentially linked to reproductive dysfunction in adulthood.

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“…In addition, a substantial number of LHRH axonal projections to other brain regions in mammals has also been reported, suggesting that the LHRH decapeptide may have other roles in addition to its classical function as a gonadotropic hormone-releasing hormone (Leonardelli and Poulain, 1977;Jennes and Stumpf, 1980;BennettClarke and Joseph, 1982;Silverman et al, 1982;Witkin et al, 1982;Silverman, 1988;Najimi et al, 1990;Sétáló et al, 1992). Moreover, in nonmammalian species, nonplacodal and placodal origins of LHRH neurons, expressed as different gene forms of LHRH, have been proposed and their specific locations have been determined (Muske, 1993;Northcutt and Muske, 1994).…”

mentioning

confidence: 93%

Spatiotemporal appearance of developing LHRH neurons in the rat brain

Daikoku

Koide

1998

J. Comp. Neurol.

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To obtain insight into the development of the heterogeneous intracerebral populations of luteinizing hormone-releasing hormone (LHRH) neurons, their spatiotemporal appearance was examined at different stages in normal rat embryos, in nasal epithelial explants in vitro, and in intrauterine nasal-operated embryos. Following the appearance of nerve cell adhesion molecule in the nasal placode at embryonic day (E) 12.5, LHRH neurons, generated in the nasal placode at E13.5, penetrated the forebrain vesicle (FV) by E14.5-15.5. After E16.5, as the FV elongated to form the olfactory bulb, the migrating neurons traversed posteriorly through the interhemispheric space to penetrate the septopreoptic (S-P) area. By E18.5, LHRH neurons were detected in the preoptic-diagonal band (P-D) area as well as in the S-P region, along with some scattered extrahypothalamic LHRH neurons. To determine the source of these neurons, we separately cultured dissected parts of E12.5 nasal pit epithelium. Neuronal generation was predominantly from the medial wall epithelium (NAP), but some LHRH neurons originated in the roof epithelium. Cocultures of the NAP (E12.5) with the FV, median eminence-arcuate complex, Rathke's pouch, mesencephalon, or medulla oblongata from E14.5 embryos revealed the ability of LHRH cells to penetrate all of these tissues. Uni- or bilateral nasal destruction was conducted at E16.5 or E15.5, respectively, and examined at E18.5 and E21.5. In the operated embryos, most LHRH neurons were present in the P-D system and some in the S-P area. This finding suggests that the neurons generated before E15.5 are primarily predisposed to form the P-D system, whereas those derived afterward form the S-P system.

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Ontogenesis of the GnRH neuron system in the rat. A quantitative immunohistochemical study with special reference to the extra cerebral GnRH-positive cells and the occupation of intracerebral termination fields

Cited by 13 publications

References 23 publications

The influence of catecholamine on the migration of gonadotropin-releasing hormone-producing neurons in the rat foetuses

The influence of catecholamine on the migration of gonadotropin-releasing hormone-producing neurons in the rat foetuses

Maternal Dexamethasone Exposure Inhibits the Gonadotropin-Releasing Hormone Neuronal Movement in the Preoptic Area of Rat Offspring

Spatiotemporal appearance of developing LHRH neurons in the rat brain

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