This study examined alterations in episodic LH release in response to prolonged, slow infusions of dopamine (DA), norepinephrine (NE), or epinephrine (EPIN) into the thire ventricle in adult, ovariectomized (OVX) rats, and the influence of priming with ovarian steroids on the LH response to the catecholamines. Unanesthetized rats with right atrial cannulae were bled continuously at slow rates for 1--1 1/2 h prior to infusion, 1--1 1/2 h during infusion, and up to 1 h afterwards. The amines were protected from oxidation by ascorbic acid, and infused in an artificial cerebrospinal fluid (CSF) vehicle (pH 7.29--7.33) into the third ventricle at a rate of 25--27 microliter/h. Blood samples were analyzed for LH by radioimmunoassay. In unprimed, OVX rats, infusions of artificial CSF, as well as low doses of DA (2--4 micrograms/h) or NE (0.3--0.6 micrograms/h), had no effect on episodic LH release or mean blood LH levels. However, administration of 8.5 and 17 micrograms DA/h, and 5.5 and 11 micrograms NE/h, resulted in a decrease in blood LH levels and, in most animals, prolonged intervals between peak blood LH levels during infusion or inhibitions which began rapidly and lasted for nearly the entire infusion period or longer. In contrast, infusion of 5.7 and 11.5 micrograms EPIN/h had no effect on blood LH levels in uprimed rats. In OVX rats primed 3 days prior to infusion with 50 micrograms estradiol benzoate and 25 mg progesterone (OEP), administration of CSF or the same doses of DA that previously inhibited episodic LH release had no effect on LH secretion. However, these steroids completely reversed the LH response to 11 micrograms NE/h, with increases in LH relase occurring during infusion. EPIN, in doses ineffective in unprimed rats (5.7 and 11.5 micrograms/h), also caused elevations in blood LH levels in EOP rats. Finally, in rats primed with 5 micrograms estradiol benzoate/100 g b.w./day for the 2 days prior to infusion, none of the three neurotransmitters had any effect on LH release.