摘要:

Hormonal modulation of pituitary gonadotropin luteinizing hormone (LH) and follicle-stimulating hormone (FSH) synthesis, as well as expression of the individual subunit genes, requires both coordinate and divergent mechanisms. Although critical roles of steroid feedback and hypothalamic gonadotropin-releasing hormone (GnRH) have been recognized for many years, subunit-specific effects of individual steroids, GnRH pulse patterns, and growth factors are becoming more defined. GnRH directly stimulates the LHβ and α-subunit genes, although mechanisms for divergent effects of specific pulse frequencies are still unknown. In contrast, GnRH stimulation of FSHβ may be mediated by gonadotrope production of activin and follistatin, which are also modulated by steroids and reproductive cycle stage. Whereas negative steroid feedback can operate by alteration of GnRH pulses, estrogen also increases pituitary sensitivity to GnRH, and testosterone directly suppresses pituitary gene expression and alters GnRH responses. Although some gonadotropin gene regions defining cell-specific expression have been localized, only a few hormonal regulatory regions and the relevant transcription factors have been identified. Future studies to characterize these genes will aid in understanding both common and divergent regulatory pathways.

ISSN:1068-3097    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

Although the negative feedback of estrogen on the hypothalamus and pituitary has been recognized for more than 60 years, the cellular mechanism by which estrogen inhibits gonadotropin-releasing hormone and gonadotropin secretion has been elusive. This review describes recent progress in our understanding of the rapid or nongenomic effects of estrogen. In particular, it has been recently found that estrogen rapidly activates a protein kinase pathway to alter synaptic transmission in hypothalamic neuropeptide neurons that directly inhibit gonadotropin-releasing hormone neurons. In addition to these rapid effects, the newly discovered biochemical pathways have the ability to alter transcription themselves, as well as to modulate the genomic effects of the classic estrogen receptor. Work is currently under way to further define the receptor and the biochemical mechanisms that mediate these rapid actions of estrogen.

ISSN:1068-3097    

出版商:OVID    

年代:1998

数据来源: OVID