Effect of allopregnanolone on glutamate release in puberty.,

GIULIANI F.; GARCÍA S.; CASAS S.; CARLA ESCUDERO; NANFARO F.; BAZZOCCHINI V.; CABRERA R.

Rosario

Congreso; XLI Reunión anual de la Sociedad Argentina de Farmacología Experimental (SAFE); 2009

SAFE

Onset of puberty in female rats, when vaginal opening becomes evident, is produced by a pulsatile GnRH release from hypothalamus. Among factors that regulate this event, Glutamatergic/NMDA system would play an essential role. Moreover, previous results of our laboratory demonstrated that this neurotransmitter system might be modulated by the neurosteroid Allopregnanolone (Allo) in adult rats. The aim of this work was to determine if Allo modify the glutamate release in hypothalamus of peripuberal and puberal rats and if this possible effect would be mediated by modulation of NMDA receptors. K+ evoked [3H]-glutamate release of medial basal hypothalamus (MBH) and preoptic area (POA) slices of peripuberal (37d approx.) and puberal (55d) rats was carried out by superfusion method. The different treatments were vehicle (KRBG Mg2+ free buffer), Allo 120nM, KRBG-Mg2+ buffer (to antagonize NMDA receptors) and KRBG-Mg2+ buffer + Allo 120nM. Results were analyzed by ANOVA 1 and Turkey’s post test (p<0.05 were considered as significant). Allo enhanced [3H]-glutamate release in both stages. The antagonism of NMDA receptors with Mg2+ reverted the Allo effect to basal values in both groups. Mg2+ alone had not effect "per se" with respect to vehicle groups. Together these data indicate that Allo would regulate glutamate release in peripuberal and puberal rats and that this effect might be mediated by NMDA receptor modulation, showing a possible new role for this neurosteroidal molecule in this important stage of reproductive life of female rats. + evoked [3H]-glutamate release of medial basal hypothalamus (MBH) and preoptic area (POA) slices of peripuberal (37d approx.) and puberal (55d) rats was carried out by superfusion method. The different treatments were vehicle (KRBG Mg2+ free buffer), Allo 120nM, KRBG-Mg2+ buffer (to antagonize NMDA receptors) and KRBG-Mg2+ buffer + Allo 120nM. Results were analyzed by ANOVA 1 and Turkey’s post test (p<0.05 were considered as significant). Allo enhanced [3H]-glutamate release in both stages. The antagonism of NMDA receptors with Mg2+ reverted the Allo effect to basal values in both groups. Mg2+ alone had not effect "per se" with respect to vehicle groups. Together these data indicate that Allo would regulate glutamate release in peripuberal and puberal rats and that this effect might be mediated by NMDA receptor modulation, showing a possible new role for this neurosteroidal molecule in this important stage of reproductive life of female rats.