Neuroendocrinology

Factors Accounting for Perinatal Occurrence of Pulsatile Gonadotropin-Releasing Hormone Secretion In Vitro in Rats

Abstract
Our aim was to study the inhibitory and facilitatory factors possibly accounting for the undetectable activity of the GnRH pulse generator in late fetal life in vitro and its awakening in early postnatal life. GABA_A receptor antagonism using SR 95 531 did not cause any secretory pulse in fetal explants whereas a significant stimulation of GnRH pulse frequency was obtained at 5 and 15 days. GnRH secretory response to repeated NMDA stimulation showed progressive disappearance indicating that the inhibitory auto-feedback was operating. GnRH release caused by glutamine was respectively 9 and 20 % of that evoked by glutamate in fetal and 5 day old rats whereas both amino acids were equally active at 15 days. Explants obtained after caesarean section performed at onset of labour did not show any secretory pulse while pulses could be observed with explants obtained 2 h after vaginal delivery. Incubation of fetal explants with oxytocin (10^-8M) or PGE₂ (10^-6M) resulted in occurrence of GnRH secretory pulses. A facilitatory effect of the oxytocin was shown to persist on day 1, 5 and 15 and inhibitory effects of an oxytocin receptor antagonist provided some evidence of endogenous oxytocin involvement. We conclude that in the fetal rat hypothalamus, GnRH inhibitory auto-feedback and GABAergic inputs do not account for the absence of pulsatile GnRH secretion in vitro. A low rate of glutamate biosynthesis from glutamine is a possibly limiting factor. Oxytocin and PGE₂ can play a facilitatory role in the postpartal occurrence of pulsatile GnRH secretion.

Key words: Neuroendocrinology • Gonadotropin-releasing hormone • Hypothalamus • Neurotransmitters • Oxytocin

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