Separate Neural Systems Mediate the Steroid-Dependent and Steroid-Independent Suppression of Tonic Luteinizing Hormone Secretion

In the ewe, two types of seasonal fluctuations in secretion of tonic luteinizing hormone (LH) have been described: a steroid-dependent change whereby estradiol gains the capacity to suppress LH pulse frequency in anestrus, and a steroid-independent decrease in pulse frequency in ovariectomized animals during anestrus. We have proposed that the former reflects activation, in anestrus, of estradiol-sensitive catecholaminergic neurons that inbi bit gonadotropin-releasing hormone (GnRH). Three results reported here support this hypothesis: 1) dopaminergic (pimozide) and a-adrenergic (pbenoxybenzamine) antagonists increased LH in intact anestrous ewes without altering pituitary responses to GnRH; 2) other dopaminergic (fluphenazine) and a-adrenergic (dibenamine) antagonists also increased LH in anestrus; 3) ago nists for dopaminergic (apomor-phine) and a-adrenergic (clonidine) receptors suppressed LH secretion in both seasons, suggesting that the appropriate receptors are present in breeding-season ewes. In contrast, catecholamines do not appear to mediate tbe steroid-independent suppression of pulse fre-quency; neither pimozide nor pbenoxybenzamine increased LH pulse frequency in ovariectomized ewes during anestrus. When antagonists for 6 other neurotransmitter receptors (muscarinic and nictotinic cholinergic, GABAnergic, serotonergic, opioid, and g3-adrenergic) were tested in anestrus, only cyprobeptadine, the seroto-nergic antagonist, increased pulse frequency in ovariectomized ewes. Cyprobeptadine bad no effect on frequency during the breeding season. On the basis of these results, we propose that the steroid-dependent and-independent actions of anestrous pbotoperiod occur via catecholaminergic and serotonergic neurons, respectively