Study summary · research use only
Astrocytes: a star emerges in the control of reproductive hormones
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This commentary discusses findings (species not specified in this text) from a related study describing kisspeptin signaling to astrocytes as another pathway influencing gonadotropin-releasing hormone (GnRH) neuronal output within the hypothalamo-pituitary-gonadal (HPG) axis. It states that astrocytes express kisspeptin receptors that activate canonical intracellular signaling to constrain kisspeptin-induced GnRH neuronal stimulation, and that appositions between kisspeptin and GnRH neurons vary across the ovarian cycle, with astrocyte kisspeptin signaling proposed as a modulator of this neuroplasticity. The commentary notes astrocyte kisspeptin signaling was also reported to mediate susceptibility to metabolic stressors and the development of obesity-induced hypogonadism.
Abstract
Kisspeptin is an essential neuropeptide sitting at the apex of the hypothalamo-pituitary-gonadal (HPG) endocrine axis to regulate gonadotropin-releasing hormone (GnRH) neurons and downstream reproductive hormones. Kisspeptin neurons integrate feedback from sex steroids facilitating regulation of the menstrual cycle and mediate the effects of metabolic stressors on the reproductive axis. In this issue of the JCI, Torres and colleagues describe another pathway for kisspeptin signaling in astrocytes to influence GnRH neuronal output. Astrocytes had kisspeptin receptors that activated canonical intracellular signaling pathways to constrain the magnitude of kisspeptin-induced GnRH neuronal stimulation. Additionally, the appositions between kisspeptin and GnRH neurons were dynamic during the ovarian cycle, with astrocyte kisspeptin signaling proposed as a putative modulator of this neuroplasticity. Importantly, astrocyte kisspeptin signaling also mediated susceptibility to metabolic stressors and the development of obesity-induced hypogonadism, underscoring the physiological and pathological importance of this pathway and revealing the importance of nonneuronal signaling in reproductive health.
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