Resumo

The role of gonadal steroids on GnRH synthesis and release is not totally clear and the GnRH content in soma and terminals of GnRH neurons represents a balance between synthesis and release. Thus, this study examined the effects of estradiol (E) and progesterone (P) on GnRH content in the preoptic area (POA) and medial basal hypothalamus (MBH). Ovariectomized rats were treated with oil or E for 3 days. On the next day, rats treated with oil were injected with oil (OVO), E (OVOE) or P (OVOP) and rats treated with E were injected with oil (OVE) or P (OVEP). Rats were decapitated at 11, 13, 15 and 17 h, brains were removed and POA and MBH punched out. Using radioimmunoassay, GnRH content was determined in the POA and MBH and plasma LH levels were measured. GnRH content and LH did not vary in OVO rats. In OVE rats APO GnRH content decreased while increased in the MBH coinciding with a small rise on LH levels. OVOE rats exhibit the same pattern though there was no LH surge. Compared to OVE, GnRH of MBH increased earlier, amplifying and advancing LH surge on OVEP rats. No changes in GnRH content or LH occurred in OVOP rats. In all E-treated rats, the increase of MBH GnRH content only in the late afternoon suggests mediation by an E dependent neural signal. P seems to potentiate this signal and to shift the neural timing, inducing GnRH release, advancing and amplifying the LH surge. Acute or chronic E treatment seems to inhibit GnRH release while P stimulating role on GnRH release requires E priming.