Semaphorin7A regulates neuroglial plasticity in the adult hypothalamic median eminence.
Semaphorin7A regulates neuroglial plasticity in the adult hypothalamic median eminence.
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DOI:
10.1038/ncomms7385
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发表时间:
2015-02-27
影响因子:
16.6
通讯作者:
Giacobini, Paolo
中科院分区:
文献类型:
--
作者:
Parkash, Jyoti;Messina, Andrea;Langlet, Fanny;Cimino, Irene;Loyens, Anne;Mazur, Daniele;Gallet, Sarah;Balland, Eglantine;Malone, Samuel A.;Pralong, Francois;Cagnoni, Gabriella;Schellino, Roberta;De Marchis, Silvia;Mazzone, Massimiliano;Pasterkamp, R. Jeroen;Tamagnone, Luca;Prevot, Vincent;Giacobini, Paolo
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. Reproduction in mammals is dependent on the function of specific neurons that secrete gonadotropin-releasing hormone (GnRH) and project their axons to the median eminence (ME) of the hypothalamus. Here the authors show that Semaphorin7A signaling plays a role in mediating the plasticity of GnRH axon terminals and tanycytes in the ME.
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影响因子:
9.8
作者:
Giacobini P;Parkash J;Campagne C;Messina A;Casoni F;Vanacker C;Langlet F;Hobo B;Cagnoni G;Gallet S;Hanchate NK;Mazur D;Taniguchi M;Mazzone M;Verhaagen J;Ciofi P;Bouret SG;Tamagnone L;Prevot V
通讯作者:
Prevot V
影响因子:
4.8
作者:
de Seranno, Sandrine;de Tassigny, Xavier d'Anglemont;Prevot, Vincent
通讯作者:
Prevot, Vincent
影响因子:
29
作者:
Balland E;Dam J;Langlet F;Caron E;Steculorum S;Messina A;Rasika S;Falluel-Morel A;Anouar Y;Dehouck B;Trinquet E;Jockers R;Bouret SG;Prévot V
通讯作者:
Prévot V
影响因子:
4.1
作者:
Bouret, S;Prevot, V;Mitchell, V
通讯作者:
Mitchell, V
影响因子:
5.3
作者:
De Seranno, S;Estrella, C;Prevot, V
通讯作者:
Prevot, V