The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 Ciofi,  
 

Phenotypical segregation among female rat hypothalamic gonadotropin-releasing hormone neurons as revealed by the sexually dimorphic coexpression of cholecystokinin and neurotensin.

The neuroendocrine control of the gonad is exerted primarily by the gonadotropin-releasing hormone neurons located in the septum and the hypothalamus. Despite their sexually dimorphic activity, tonic in males and phasic in females, these neurons have not appeared qualitatively different between sexes in intrinsic organization or chemical phenotype. Here, by using multiple-label immunocytochemistry, it is demonstrated that the phenotype of gonadotropin-releasing hormone neurons is sex specific. In females only, 54.5% of them co-expressed cholecystokinin immunoreactivity and 29.4% additionally expressed neurotensin immunoreactivity. These multipeptidergic neurons were observed in the hypothalamus but not in the septum. During postnatal development, cholecystokinin and neurotensin immunoreactivities were first detected in gonadotropin-releasing hormone-containing axons of the median eminence at vaginal opening, suggesting an involvement of the neuropeptides in peri-ovulatory events. This peptidergic phenotype was not apparent in females ovariectomized as adults but was reinstated by estradiol treatment. In adult males, the testicle does not control this phenotype because orchidectomized adults did not display it, whatever the post-operative delay (one to five weeks) or substitutive chronic steroid treatment (testosterone or estradiol). The testicle may, however, masculinize the phenotype neonatally because estradiol or testosterone treatment in adulthood induced an expression of cholecystokinin immunoreactivity in gonadotropin-releasing hormone-containing axons of the median eminence in both males and females that were gonadectomized at birth. This procedure, however, failed to significantly induce an expression of neurotensin immunoreactivity, suggesting a role of the postnatal ovary on this element of the chemistry of gonadotropin-releasing hormone neurons.Thus, the gonad permanently organizes the gonadotropin-releasing hormone neuronal population, resulting, at least in females, in a mosaic of phenotypically distinct, functional subunits.[1]

References

 
WikiGenes - Universities