Separate Neural Systems Mediate the Steroid-Dependent and Steroid-Independent Suppression of Tonic Luteinizing Hormone Secretion in the Anestrous Ewe1

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Abstract
In the ewe, two types of seasonal fluctuations in secretion of tonic lutenizing 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, or estradiol-sensitive catecholaminergic neurons that inhibit gonadotropin-releasing hormone (GnRH). Three results reported there support this hypothesis: 1) dopaminergic (pimozide) and .alpha.-adrenergic (phenoxybenzamine) antagonists increased LH in intact anestrous ewes without altering pituitary responses to GnRH; 2) other dopaminergic (fluphenazine) and .alpha.-adrenergic (dibenamine) antagonists also increased LH in anestrus; 3) agonists for dopaminergic (apomorphine) and .alpha.-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 the steroid-independent suppression of pulse frequency; neither pimozide nor phenoxybenzamine increased LH pulse frequency in ovariectomized ewes during anestrus. When antagonists for 6 other neurotransmitter receptors (muscarinic and nictotinic cholinergic, GABAnergic, serotonergic, opioid, and .beta.-adrenergic) were tested in anestrus, only cyproheptadine, the serotonergic antagonist, increased pulse frequency in ovariectomized ewes. Cyproheptadine had 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 photoperiod occur via catecholaminergic and serotonergic neurons, respectively.