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Increased Vesicular γ‐GABA Transporter and Decreased Phosphorylation of Synapsin I in the Rostral Preoptic Area is Associated with Decreased Gonadotrophin‐Releasing Hormone and c‐F os Coexpression in Middle‐Aged Female Mice
Author(s) -
Zhang Jing,
Yang L. M.,
Pan X. D.,
Lin N.,
Chen X. C.
Publication year - 2013
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1111/jne.12050
Subject(s) - medicine , endocrinology , preoptic area , synapsin , gonadotropin releasing hormone , synapsin i , glutamate receptor , hypothalamus , biology , luteinizing hormone , hormone , neurotransmission , estrous cycle , neurotransmitter , synaptic vesicle , receptor , central nervous system , vesicle , biochemistry , membrane
Hypothalamic glutamate (Glu) and γ‐GABA neurotransmission are involved in the ovarian hormone‐induced gonadotrophin‐releasing hormone (GnRH)/luteinising hormone (LH) surge in rodents. Studies have shown that reduced Glu and increased γ‐GABA in the rostral preoptic area (rPOA) of the hypothalamus, where most activated GnRH neurones are located, play a key role in decreasing the reproductive function of female rats. However, the mechanism underlying the altered balance of these neurotransmitters is poorly understood. In the present study, we observed a decline in the function of GnRH neurones in the rPOA at the time of the GnRH/LH surge in middle‐aged intact female mice with regular oestrous cycles. In young mice, there is an increase of vesicular Glu transporter 2 on the pro‐oestrus afternoon, which is not observed in middle‐aged mice. By contrast, vesicular γ‐GABA transporter levels in young mice decrease at the time of the LH surge, whereas they increase in middle‐aged mice. Of note, we found that, in middle‐aged mice at the time of the GnRH/LH surge, the phosphorylation of synapsin I at Ser603 and Ca 2+ /calmodulin‐dependent kinase IIα was significantly lower than in young mice. These data suggest that, in middle‐aged mice, higher levels of presynaptic stores of GABA, a lack of increase of Glu and a decreased ability of synaptic vesicle mobilisation could account for the imbalance of Glu and GABA in the rPOA, which decreases the activation of GnRH neurones.