Adult female rats were implanted with permanent cannulae in the third ventricle of the brain and allowed to recover regular 4-day estrous cycles. They received intrajugular cannulae on the morning of proestrus and later between 12.00–13.00 h catecholamines – norepinephrine (NE; 5.3 or 15.9 µg), dopamine (DA; 5.3 µg), epinephrine (E; 5.3 or 15.9 µg) or vehicle (artificial CSF) – were administered intraventricularly. Plasma LH levels were measured in blood samples obtained prior to and 10, 20, 30 or 60 min after catecholamine injections. While NE or DA failed to alter basal plasma LH levels, E evoked a significant 2-fold rise in plasma LH levels. Quite unexpectedly, however, infusion of E (18.5 µg) over a 30-min period during the critical period failed to either reverse the pentobarbital-blockade of ovulation or stimulate LH release. Prior suppression of E levels selectively with LY 78335 blocked the preovulatory LH surge and ovulation. However, intraventricular E failed to evoke LH release in these LY 78335-blocked proestrous rats, an observation suggestive of some α1-adrenoreceptor blocking action of the drug. In contrast, the α1-adrenoreceptor blocking action was not evident in the estrogen, progesterone-primed ovariectomized rats similarly pretreated with LY 78335. These studies show that (1) E-containing neurons in the hypothalamus may play an important role in the preovulatory LH release; (2) LY 78335 may exert inhibitory effects on preovulatory LH release, in part, by blocking α1-adrenoreceptors, and (3) participation of NE and DA, if any, in evoking preovulatory LH release remains to be