Ratra Dhirender V, Elias Carol F
Department of Molecular & Integrative Physiology, University of Michigan, Ann Arbor, MI 48109, USA.
Department of Molecular & Integrative Physiology, University of Michigan, Ann Arbor, MI 48109, USA; Department of Obstetrics and Gynecology, University of Michigan, Ann Arbor, MI 48109, USA.
J Chem Neuroanat. 2014 Nov;61-62:233-8. doi: 10.1016/j.jchemneu.2014.05.005. Epub 2014 Jun 7.
The adipocyte-derived hormone leptin plays a critical role as a metabolic cue for the reproductive system. Conditions of low leptin levels observed in negative energy balance and loss-of-function mutations of leptin or leptin receptor genes are characterized by decreased fertility. In recent years, advances have been made for identifying possible hypothalamic neurons relaying leptin's neuroendocrine control of reproductive function. Studies from different laboratories have demonstrated that leptin action in the hypothalamo-pituitary-gonadal (HPG) axis is exerted via hypothalamic interneurons regulating gonadotropin-releasing hormone (GnRH) cells, oppose to direct action on GnRH neurons. Following this observation, studies focused on identifying leptin responsive interneurons. Using a Cre-loxP system to re-express or delete the leptin receptor long form (LepRb) from kisspeptin neurons, our laboratory found that leptin's action on kiss1 cells is neither required nor sufficient for leptin's role in reproductive function. Endogenous re-expression of LepRb however, in glutamatergic neurons of the ventral premammilary nucleus (PMV) or ablation of agouti-related protein (AgRP) neurons from leptin signaling-deficient mice are both sufficient to induce puberty and improve fertility. Recent studies have also shown that leptin action in first order GABAergic neurons is required for fertility. Together, these studies begin to delineate key neuronal populations involved in leptin's action in reproduction. In this review, we discuss recent advances made in the field and highlight the questions yet to be answered.
脂肪细胞衍生的激素瘦素作为生殖系统的代谢信号发挥着关键作用。在负能量平衡以及瘦素或瘦素受体基因功能丧失突变中观察到的低瘦素水平状况,其特征是生育能力下降。近年来,在确定传递瘦素对生殖功能神经内分泌控制的可能下丘脑神经元方面取得了进展。来自不同实验室的研究表明,瘦素在下丘脑 - 垂体 - 性腺(HPG)轴中的作用是通过调节促性腺激素释放激素(GnRH)细胞的下丘脑中间神经元来发挥的,而不是直接作用于GnRH神经元。基于这一观察结果,研究集中于识别对瘦素作出反应的中间神经元。利用Cre-loxP系统在亲吻素神经元中重新表达或删除瘦素受体长型(LepRb),我们实验室发现,瘦素对kiss1细胞的作用对于瘦素在生殖功能中的作用既非必需也不充分。然而,在腹内侧乳头体前核(PMV)的谷氨酸能神经元中内源性重新表达LepRb,或从瘦素信号缺陷小鼠中切除刺鼠相关蛋白(AgRP)神经元,都足以诱导青春期并提高生育能力。最近的研究还表明,生育能力需要瘦素在一级GABA能神经元中的作用。总之,这些研究开始描绘出参与瘦素生殖作用的关键神经元群体。在这篇综述中,我们讨论了该领域最近取得的进展,并突出了有待解答的问题。