An involvement of catecholamines in the preovulatory gonadotropin surge has been proposed for many years. Specifically, an α-adrenergic mechanism has been implicated in the stimulation of ovulation and LH release. On the other hand, little is known regarding the possible role of adrenergic neurotransmission once a gonadotropin surge has been initiated. In this study, drugs which affect adrenergic receptors were administered centrally to estrogen-primed ovariectomized rats and the effects on serum concentrations of LH and FSH induced by treatment with progesterone at 08.00 h were examined. As expected, the progesterone treatment caused a significant (p < 0.05) increase in blood LH and FSH levels by 14.00 and 15.00 h, respectively, when compared with those seen at 13.00 h. In control rats that received isotonic saline intraventricularly at 15.00–16.00 h, both LH and FSH levels continued to rise linearly and reached peak levels by 17.00 and 18.00 h. By contrast, intraventricular infusion of norepinephrine at 16.00 h caused a significant decrease (p<0.05) in LH levels when compared with the saline-infused control groups. Moreover, rats that received intraventricular infusion of phenylephrine (an α1-adrenergic agonist) at 15.00 h failed to show a significant increase in LH and FSH levels until 19.00 h; this inhibitory effect was mimicked by a relatively more specific α1-adrenergic agonist, methoxamine. Consistent with our previous findings, animals which received intraventricular isoproterenol (a specific β-adrenergic agonist) at 15.00 h also responded with suppressed serum LH levels at 16.00–19.00 h when compared with controls. Thus, in addition to the well-known stimulatory role of NE and α-adrenergic agonists for the onset of the LH/FSH surge, these rather unexpected data suggest that α1-adrenergic neurotransmitters may have a dual and paradoxical role and actually attenuate LH and FSH release (even in a steroid-primed environment) once a gonadotropin surge has been