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Anna Cariboni

Publications and source records attributed to Anna Cariboni.

5 recordsLinked to original sources
PubMed2006

Expression and differential effects of the activation of glucocorticoid receptors in mouse gonadotropin-releasing hormone neurons.

Prenatal exposure of rodents to glucocorticoids (Gc) affects the sexual development of the offspring, possibly interfering with the differentiation of the hypothalamic-pituitary-gonadal axis. Glucocorticoid receptors (GR) are present on gonadotropin-releasing hormone (GnRH) neurons in the rat hypothalamus, suggesting a direct effect of Gc in the control of the synthesis and/or release of the hormone. In this study, we demonstrate the colocalization of immunoreactive GR with GnRH in a subpopulation of mouse hypothalamic GnRH neurons, confirming the possible involvement of Gc in mouse GnRH neuronal physiology. Receptor-binding assay, RT-PCR, immunocytochemistry, and immunoblotting experiments carried out in GN11 immortalized GnRH neurons show the presence of GR even in the more immature mouse GnRH neurons and confirm the expression of GR in GT1-7 mature GnRH cells. In GN11 cells, the activation of GR with dexamethasone produces nuclear translocation, but does not lead to the inhibition of GnRH gene expression already reported in GT1-7 cells. Long-term exposure of GN11 cells to dexamethasone induces an epithelial-like phenotype with a reorganization of F-actin in stress fibers. Finally, we found that Gc treatment significantly decreases the migratory activity in vitro and the levels of phosphorylated focal adhesion kinase of GN11 immature neurons. In conclusion, these data indicate that GR are expressed in mouse hypothalamic GnRH neurons in vivo as well as in the immature GN11 GnRH neurons in vitro. Moreover, the effects of the GR activation in GN11 and in GT1-7 cells may be related to the neuronal maturational stage of the two cell lines, suggesting a differential role of Gc in neuronal development.

Age Factors↗
PubMed2005

Reelin provides an inhibitory signal in the migration of gonadotropin-releasing hormone neurons.

Gonadotropin-releasing hormone (GnRH) neurons, a small number of cells scattered in the hypothalamic region of the basal forebrain, play an important role in reproductive function. These cells originate in the olfactory placode and migrate into the basal forebrain in late embryonic life. Here, we show that reelin, which is expressed along the route of the migrating cells, has an inhibitory role in guiding GnRH neurons to the basal forebrain. Only a small (approximately 5%) subpopulation of these neurons expresses one of the reelin receptors (ApoER2/Lrp8), and all GnRH neurons appear to lack the intracellular adaptor protein Dab1, suggesting that the function of reelin is not mediated by the conventional signal transduction pathway. The importance of reelin in the establishment of GnRH neurons in the hypothalamus was confirmed by our finding that the brains of developing and adult reeler mice of both sexes contained a markedly reduced number of these neuroendocrine neurons. Furthermore, the testes of adult males showed dilation of seminiferous tubules and reduction in their density when compared with controls. Mutants lacking the reelin receptors ApoER2 and Vldlr, and scrambler mice lacking Dab1, showed a normal complement of GnRH neurons in the hypothalamus, confirming that the effect of reelin in their migration is independent of Dab1.

Animals↗
PubMed2004

The product of X-linked Kallmann's syndrome gene (KAL1) affects the migratory activity of gonadotropin-releasing hormone (GnRH)-producing neurons.

X-linked Kallmann's syndrome (KS) is a genetic disease characterized by anosmia and hypogonadism due to impairment in the development of olfactory axons and in the migration of gonadotropin-releasing hormone (GnRH)-producing neurons. Deletions or point mutations of a gene located at Xp22.3 (KAL1) are responsible for the disease. This gene encodes for a secreted heparin-binding protein (KAL or anosmin-1) which exhibits similarities with cell-adhesion molecules. In the present study, we show for the first time a direct action of anosmin-1 on the migratory activity of GnRH neurons. Specifically, we exposed immortalized migrating GnRH neurons (GN11 cells) to conditioned media (CM) of COS or CHO cells transiently transfected with human KAL1 gene in microchemotaxis and collagen gel assays. We found that anosmin-1-enriched media produced a cell-specific chemotactic response of GN11 cells. None of the CM enriched on three forms of anosmin-1 carrying different missense mutations (N267K, E514K and F517L) found in patients affected by X-linked KS affected the chemomigration of GN11 cells. Anosmin binds to the GN11 cell surface by interacting with the heparan sulphate proteoglycans, and the chemotactic effect of anosmin-1-enriched CM can be specifically blocked by heparin or by heparitinase pretreatment. These results strongly suggest an involvement of anosmin-1 in the control of the migratory behaviour of GnRH neurons and provide novel information on the pathogenesis of KS.

Animals↗
PubMed2003

Depolarization differentially affects the secretory and migratory properties of two cell lines of immortalized luteinizing hormone-releasing hormone (LHRH) neurons.

In this report we studied and compared the biochemical and the electrophysiological characteristics of two cell lines (GT1-7 and GN11) of immortalized mouse LHRH-expressing neurons and the correlation with their maturational stage and migratory activity. In fact, previous results indicated that GN11, but not GT1-7, cells exhibit an elevated motility in vitro. The results show that the two cell lines differ in terms of immunoreactivity for tyrosine hydroxylase and nestin as well as of production and release of 3,4-dihydroxyphenylalanine (DOPA) and of intracellular distribution and release of the LHRH. Patch-clamp recordings in GN11 cells, reveal the presence of a single inward rectifier K+ current indicative of an immature neuronal phenotype (neither firing nor electrical activity). In contrast, as known from previous studies, GT1-7 cells show the characteristics of mature LHRH neurons with a high electrical activity characterized by spontaneous firing and excitatory postsynaptic potentials. K+-induced depolarization induces in GT1-7 cells, but not in GN11 cells, a strong increase in the release of LHRH in the culture medium. However, depolarization of GN11 cells significantly decreases their chemomigratory response. In conclusion, these results indicate that GT1-7 and GN11 cells show different biochemical and electrophysiological characteristics and are representative of mature and immature LHRH neurons, respectively. The early stage of maturation of GN11 cells, as well as the low electrical activity detected in these cells, appears to correlate with their migratory activity in vitro.

Anesthetics, Local↗