Abstract
The possibility that biogenic amines play a physiological role in the spontaneous regulation of luteinizing hormone (LH) release was first indicated by Sawyer, Everett and Markee in 1949. They demonstrated that rats treated with dibenamine, an α-adrenergic receptor blocking drug, failed to ovulate (Sawyer et al., 1949; Everett et al., 1949; Everett and Sawyer, 1949). A thorough development of their original research became possible only with the introduction of the radioimmunoassay for LH twenty years later. By 1976 it had been established that an increased discharge of LH releasing hormone (LHRH) into pituitary portal blood on the day of proestrus causes a marked surge in the systemic concentration of LH and results in ovulation (Sarkar et al., 1976). This surge is entrained to the light-dark cycle and its occurrence (peaking at approximately 1800 h with lighting from 0600 to 2000 h) depends upon an elevated level of serum estrogen and a central circadian “clock” which is probably located in the suprachiasmatic nuclei of the hypothalamus (Coen and MacKinnon, 1976, 1977, 1980; Raisman and Brown-Grant, 1977). In 1976 there was also the first report clearly indicating that the majority of the LHRH-containing perikarya which project to the median eminence in the rat are located in the medial preoptic area near the organum vasculosum of the lamina terminalis (Setalo et al., 1976).
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