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Effects of 500nm polystyrene nanoplastic exposure on immortlized GnRH neurons

ABSTRACT: Plastic pollution, especially from mismanaged waste degrading into nanoplastics (NPs), poses a growing threat to environmental and human health. Polystyrene NPs (PS-NPs) are particularly prevalent, infiltrating ecosystems and accumulating in organs, including the brain. While NPs are linked to behavioral, metabolic, and developmental effects, their impact on reproduction and fertility remains poorly understood. Declining fertility rates suggest environmental toxicants like NPs may contribute to adverse reproductive outcomes. Reproductive function relies on the hypothalamus-pituitary-gonad (HPG) axis, centrally regulated by gonadotropin-releasing hormone (GnRH) neurons. These neurons originate in the nasal placode and migrate to the hypothalamus during embryogenesis. Altered GnRH neuron development or release can lead to absent puberty and infertility, whose genetic causes explain only 50% of known cases. In this context, environmental factors including NPs might contribute to the etiology of these disorders. In this work, we take advantage of an established model of migrating GnRH neurons (GN11) to assess PS-NPs effects and to provide the first evidence that these environmental factors interfere with cellular and molecular processes of GnRH neurons, thus suggesting a novel mechanism contributing to idiopathic infertility.

ORGANISM(S): Mus musculus

PROVIDER: GSE295898 | GEO | 2026/03/10

REPOSITORIES: GEO

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Project description:Fertility critically depends on the gonadotropin-releasing hormone (GnRH) pulse generator, a neural construct comprised of hypothalamic neurons coexpressing kisspeptin, neurokoinin-B and dynorphin. Here, using mathematical modeling and in vivo optogenetics we reveal for the first time how this neural construct initiates and sustains the appropriate ultradian frequency essential for reproduction. Prompted by mathematical modeling, we show experimentally using female estrous mice that robust pulsatile release of luteinizing hormone, a proxy for GnRH, emerges abruptly as we increase the basal activity of the neuronal network using continuous low-frequency optogenetic stimulation. Further increase in basal activity markedly increases pulse frequency and eventually leads to pulse termination. Additional model predictions that pulsatile dynamics emerge from nonlinear positive and negative feedback interactions mediated through neurokinin-B and dynorphin signaling respectively are confirmed neuropharmacologically. Our results shed light on the long-elusive GnRH pulse generator offering new horizons for reproductive health and wellbeing.SIGNIFICANCE STATEMENT The gonadotropin-releasing hormone (GnRH) pulse generator controls the pulsatile secretion of the gonadotropic hormones LH and FSH and is critical for fertility. The hypothalamic arcuate kisspeptin neurons are thought to represent the GnRH pulse generator, since their oscillatory activity is coincident with LH pulses in the blood; a proxy for GnRH pulses. However, the mechanisms underlying GnRH pulse generation remain elusive. We developed a mathematical model of the kisspeptin neuronal network and confirmed its predictions experimentally, showing how LH secretion is frequency-modulated as we increase the basal activity of the arcuate kisspeptin neurons in vivo using continuous optogenetic stimulation. Our model provides a quantitative framework for understanding the reproductive neuroendocrine system and opens new horizons for fertility regulation Model is encoded by Johannes and submitted to BioModels by Ahmad Zyoud.

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Effects of 500nm polystyrene nanoplastic exposure on immortlized GnRH neurons

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