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Erratum: Effect of Ovarian Hormones on the Hypothalamic Excitatory Amino Acids System during Sexual Maturation in Female Rats

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posted on 25.07.2017, 13:31 by Carbone S., Szwarcfarb B., Losada M., Moguilevsky J.A.
The present experiments were designed to study in female rats during sexual maturation: (1) the hypothalamic release of aspartate (Asp), glutamate (Glu) and glycine (Gly) which are the excitatory amino acids (EAAs) involved in NMDA neurotransmission and of taurine (Tau), a putative inhibitory amino acid of GnRH secretion; (2) the relationships between the effect of estrogen-progesterone (EP) on the release of these EAAs and the secretion of gonado-tropins, and (3) the effect of hypothalamic NMDA receptor stimulation on EAAs release by the hypothalamus as well as the effect of EP on this release. The release of EAAs by the anterior preoptic and medial-basal hypothalamic areas (APOA-MBH) is significantly higher in peripubertal than in prepubertal rats (p < 0.01). EP treatment in prepubertal rats (16 days of age) decreased LH and FSH plasmatic levels and also the in vitro release of Asp, Glu, Gly and Tau. Contrary to the observations in prepubertal rats, in 30-day-old peripubertal rats the ovarian hormones significantly (p < 0.01) increased the levels of LH and FSH as well as the release to the medium of these amino acids. In prepubertal rats, the addition of NMDA to the incubation media significantly increased the release of Asp and of Glu. The NMDA receptor agonist did not modify the hypothalamic release of Gly and Tau to the incubation media. On the other hand, pretreatment with EP did not modify either the Asp and Glu release response to NMDA or the lack of response on Gly and Tau. In peripubertal rats NMDA also significantly increased the in vitro release of Asp and Glu, but at this age pretreatment with EP significantly potentiated the release of these amino acids induced by NMDA. On the other hand, the ovarian hormones induced Gly and Tau release by NMDA, this not being observed in control rats. In conclusion, the present results indicate that during sexual maturation the in vitro release of Asp, Glu and Gly by APOA-MBH increases and Tau release decreases. EP pretreatment of prepubertal rats decreases the hypothalamic release of EAAs as well as the serum LH and FSH levels but increases both EAAs release and plasmatic gonadotropin in peripubertal rats. On the basis of these results it is proposed that the increase in EAAs release by the hypothalamus is directly connected with the onset of puberty and that the maturation of the positive feedback effect of ovarian hormones on gonadotropin secretion is related to the maturation of the capacity of EP to increase hypothalamic EAAs. Before this maturational event EP inhibits EAAs release as well as gonadotropin release (prepubertal rats). NMDA receptor stimulation leads to a positive mechanism which increases the release of Asp and Glu from APOA-MBH both in prepubertal and peripubertal rats, but EP potentiates this mechanism only in peripubertal rats. This could be an additional neuroendocrine mechanism involved in the increase of gonadotropin during sexual maturation which induces the onset of puberty and the preovulatory discharge of these pituitary hormones.