The control of LHRH release by catecholamine systems during fetal life (embryonic stages) was studied using hypothalamic neurons in primary cell cultures and an attempt was made to characterize the receptor type involved. Phenylephrine and clonidine, respectively alpha 1 an alpha 2 adrenoreceptor agonists, both inhibited LHRH release. These agonist inhibitory induced-effects were antagonized by the respective alpha 1 and alpha 2 adrenoreceptor antagonists (prazosin and rauwolscine). Both prazosin and rauwolscine applied alone induced a marked increase in LHRH release. Similarly, inhibition of catecholamine synthesis obtained by alpha-methyl-para-tyrosine (alpha-MT) led to a significant increase in LHRH release. The stimulatory effects induced by alpha 1 and alpha 2 adrenoreceptor antagonists or by alpha-MT on LHRH release suggest the presence of noradrenergic and/or adrenergic cells in fetal hypothalamic cultures. Therefore, catecholamine contents were measured in fetal hypothalamic cells in culture. Measurable amounts of norepinephrine and dopamine were found in cells, although epinephrine was undetectable. These results show: 1--noradrenergic cells are present in primary culture of fetal hypothalamic cells. 2--This intrinsic hypothalamic noradrenergic system exerts an inhibitory control on LHRH release at an early stage of development through alpha 1 and alpha 2 adrenoreceptors.