ESPEYB19 7. Puberty Basic Science (7 abstracts)
7.8. GnRH neurons recruit astrocytes in infancy to facilitate network integration and sexual maturation
Pellegrino G , Martin M , Allet C , Lhomme T , Geller S , Franssen D , Mansuy V , Manfredi-Lozano M , Coutteau-Robles A , Delli V , Rasika S , Mazur D , Loyens A , Tena-Sempere M , Siepmann J , Pralong FP , Ciofi P , Corfas G , Parent AS , Ojeda SR , Sharif A & Prevot V
Nat Neurosci. 2021 Dec;24(12):1660-1672. doi: 10.1038/s41593-021-00960-z. Epub 2021 Nov 18. PMID: 34795451. https://www.nature.com/articles/s41593-021-00960-z
Brief Summary: This neuroanatomical and physiological study in mice demonstrates that GnRH neurons attract glial cells in their vicinity via cell–cell communication during postnatal development, which is essential for proper reproductive function in adulthood.
The glial environment of GnRH neurons is essential for the regulation of GnRH release and reproductive function [1]. The mechanisms involved in the establishment of this glial microenvironment are still unknown. Based on the evidence that in the neocortex astrocyte formation in the neocortex is regulated by extrinsic signals generated by neurons [2], the authors hypothesized that GnRH neurons could be responsible for the recruitment of glial cells in their vicinity during postnatal development. By mapping cell proliferation in the preoptic area during mouse postnatal development, they determined that the progenitors associated to GnRH neurons would mainly generate astrocytes. Blocking gliogenesis with an anti-mitotic led to delayed sexual maturation in female mice. Postnatal exposure to the endocrine disruptor bisphenol A similarly delayed puberty and disrupted the abililty of GnRH neurons to recruit progenitors. Using in vitro assays, the authors discovered that GnRH neurons responded to incoming glial signals by synthesizing prostaglandin D2 (PGD2). Inhibition of PGD2 receptor in the preoptic area during infantile period led to alterations of GnRH neuron firing, disruption of minipuberty and delayed acquisition of reproductive capacity in female mice.
This study reveals a new neuron-to-neural-progenitor communication process that is essential for the postnatal development of the glial environment of GnRH neurons and for proper reproductive function in female mice. Moreover, this process can be altered by EDC treatment and lead to disrupted puberty/reproduction.
References: 1. Clasadonte, J., Prevot, V. (2018) “The special relationship: glia–neuron interactions in the neuroendocrine hypothalamus.” Nat. Rev. Endocrinol; 14:25–44. 2. Barnabe-Heider, F. et al. (2005) “Evidence that embryonic neurons regulate the onset of cortical gliogenesis via cardiotrophin-1.” Neuron 48, 253–265.
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ESPE Yearbook of Paediatric Endocrinology
ISSN 1662-4009 (Online)
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