Abstract
Reproduction is associated with the circadian system, primarily as a result of the connectivity between the biological clock in the suprachiasmatic nucleus (SCN) and reproduction-regulating brain regions, such as preoptic area (POA), anteroventral periventricular nucleus (AVPV), and arcuate nucleus (ARC). Networking of the central pacemaker to these hypothalamic brain regions is partly represented by close fiber appositions to specialized neurons, such as kisspeptin and gonadotropin-releasing hormone (GnRH) neurons; accounting for rhythmic release of gonadotropins and sex steroids. Numerous studies have attempted to dissect the neurochemical properties of GnRH neurons, which possess intrinsic oscillatory features through the presence of clock genes to regulate the pulsatile and circadian secretion. However, less attention has been given to kisspeptin, the upstream regulator of GnRH and a potent mediator of reproductive functions including puberty. Kisspeptin exerts its stimulatory effects on GnRH secretion via its cognate Kiss-1R receptor that is co-expressed on GnRH neurons. Emerging studies have found that kisspeptin neurons oscillate on a circadian basis and that these neurons also express clock genes that are thought to regulate its rhythmic activities. Based on the fiber networks between the SCN and reproductive nuclei such as the POA, AVPV, and ARC, it is suggested that interactions among the central biological clock and reproductive neurons ensure optimal reproductive functionality. Within this neuronal circuitry, kisspeptin neuronal system is likely to “time” reproduction in a long term during development and aging, in a medium term to regulate circadian or estrus cycle, and in a short term to regulate pulsatile GnRH secretion.
Highlights
Reproduction, a central feature of life, requires synergistic actions of cellular processes at the brain and the reproductive organs to achieve normal sexual functionalities
The findings suggest that agerelated reproductive neuroendocrine deficiencies originate from a loss of response of kisspeptin neurons in anteroventral periventricular nucleus (AVPV) to estrogenic signals, altering its secretory pattern and disrupting stimulation of the HPG axis [69]
Central administration of Dyn inhibited multiple-unit activity (MUA) in the medial basal hypothalamus and pulsatile luteinizing hormone (LH) secretion, whereas neurokinin B (NKB) induced MUA and pulsatile LH secretion [135]. These results suggest that arcuate nucleus (ARC) kisspeptin neurons regulate pulsatile gonadotropin-releasing hormone (GnRH)/LH secretion acting with NKB and Dyn in the ARC
Summary
Reproduction, a central feature of life, requires synergistic actions of cellular processes at the brain and the reproductive organs to achieve normal sexual functionalities. When kisspeptin is bound to its cognate G-protein-coupled receptor (GPR) 54, commonly known as Kiss1-R, to stimulate GnRH secretion, the release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from gonadotropes occurs [6] This process culminates in the synthesis of sex steroids at the gonads and, in concert with the action of gonadotropins, stimulates gametogenesis [10,11,12] (Figure 1). Rhythmicity of GnRH neuronal activity and reproductive hormonal fluctuation are studied well in female rodents During their estrous cycle (metestrous, diestrus, proestrus, and estrus), which normally cycles in 4–5 days in rats and mice, estradiol secreted from the ovary gradually increases until proestrus stage and rapidly decreases at estrus stage. Kisspeptin neuronal system is likely to “time” reproduction during development and aging by regulating circadian or estrus reproductive cycle as well as pulsatile GnRH/LH secretion
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