It has been reported that the corticomedial amygdala (CMA) is involved in regulating various hypothalamic and neuroendocrine events. This study examined the role of the CMA in the regulation of the nocturnal surge of prolactin (PRL) induced by cervical stimulation (CS). Female Sprague-Dawley rats were ovariectomized, received CMA or sham lesions, and were placed on a reversed lighting schedule of 14 h light: 10 h dark. 3 weeks later, all rats were cervically stimulated. 5 days after CS (CS + 5) rats were fitted with chronic, intraatrial catheters, and daily progesterone (P) injections (10 mg s.c.) were initiated. On CS + 8, CS + 12, and CS + 15, sequential blood samples were taken from unrestrained rats at 00.00, 02.00, 04.00, 06.00, 08.00, and 10.00 h (animal time). CMA lesions significantly reduced peak PRL levels on CS + 12 and CS+ 15, but not on CS + 8. When ovariectomized CS rats received either 1 or 10 mg P/day and were sampled on CS+ 12, CS+ 15, and CS + 19, CMA lesions reduced the magnitude of the surge on CS+ 12 and CS + 15, a time when P amplification of the surge was apparent. On CS+ 19, when P amplification of the surge was absent, CMA lesions had no effect. CMA lesions greatly reduced peak PRL levels on CS + 12, but not on CS + 8, when rats were lesioned, catheterized, and injected daily with 1 or 10 mg P/day on CS + 3. Similar results were seen in CS rats with their ovaries intact. CMA lesions reduced the magnitude of the nocturnal PRL surge on CS + 12, but not on CS + 8, in pseudopregnant rats that were given 2 mg P/day, in addition to their ovarian P secretion, to extend the occurrence of the surge through CS+ 12. Since lesions of the CMA resulted in blocking the extension of the amplitude of the nocturnal surge, it is suggested that the CMA may play a role in the termination process of the surge. The CMA may mediate at least part of the action of P to delay termination of the surge.