Send to

Choose Destination
Nat Commun. 2015 Feb 27;6:6385. doi: 10.1038/ncomms7385.

Semaphorin7A regulates neuroglial plasticity in the adult hypothalamic median eminence.

Author information

1] Inserm, Laboratory of Development and Plasticity of the Neuroendocrine Brain, Jean-Pierre Aubert Research Centre, U1172, 59045 Lille, France [2] University of Lille, School of Medicine and Institut de Medecine Predictive et de Recherche Therapeutique (IMPRT-IFR114), 59045 Lille, France.
Service of Endocrinology, Diabetology and Metabolism, Faculty of Biology and Medicine, University Hospital, 1011 Lausanne, Switzerland.
1] Candiolo Cancer Institute-FPO, IRCCS, 10060 Candiolo, Italy [2] Department of Oncology, University of Torino, 10060 Candiolo, Italy.
Dipartimento di Scienze della Vita e Biologia dei Sistemi, University of Torino, 10100 Torino, Italy.
1] Laboratory of Molecular Oncology and Angiogenesis, Vesalius Research Center, VIB, B-3000 Leuven, Belgium [2] Laboratory of Molecular Oncology and Angiogenesis, Vesalius Research Center, Department of Oncology, KU Leuven, B-3000 Leuven, Belgium.
Department of Translational Neuroscience, Brain Center Rudolf Magnus, University Medical Center Utrecht, 3584 CG11 Utrecht, The Netherlands.


Reproductive competence in mammals depends on the projection of gonadotropin-releasing hormone (GnRH) neurons to the hypothalamic median eminence (ME) and the timely release of GnRH into the hypothalamic-pituitary-gonadal axis. In adult rodents, GnRH neurons and the specialized glial cells named tanycytes periodically undergo cytoskeletal plasticity. However, the mechanisms that regulate this plasticity are still largely unknown. We demonstrate that Semaphorin7A, expressed by tanycytes, plays a dual role, inducing the retraction of GnRH terminals and promoting their ensheathment by tanycytic end feet via the receptors PlexinC1 and Itgb1, respectively. Moreover, Semaphorin7A expression is regulated during the oestrous cycle by the fluctuating levels of gonadal steroids. Genetic invalidation of Semaphorin7A receptors in mice induces neuronal and glial rearrangements in the ME and abolishes normal oestrous cyclicity and fertility. These results show a role for Semaphorin7A signalling in mediating periodic neuroglial remodelling in the adult ME during the ovarian cycle.

[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center