Abstract
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.
Highlights
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
As Sema7A is expressed postnatally in the ME18, where GnRH terminals secrete their neurohormone, we investigated whether this signalling molecule could play a role in the correct functioning of the GnRH system during adulthood
GnRH nerve terminals are located in close proximity to the pericapillary space of pituitary portal blood vessels in the ME during proestrus, in preparation for neurohormone release, but they retract during diestrus[19] as well as after gonadectomy[20], when GnRH secretion is low
Summary
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. 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. We have recently shown that Semaphorin7A (Sema7A) is essential for the development of the GnRH neuronal system, and that loss of Sema7A signalling during early development alters GnRH neuron migration, resulting in significantly reduced numbers of these neurons in the adult brain as well as in reduced gonadal size and subfertility[15,16] These molecules are constitutively expressed in the postnatal brain and could regulate neuronal plasticity and nervous system physiology in adulthood[14,17]. We show that tanycytes play an active role in mammalian reproduction via Sema7A/Itgb[1] signalling
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