Abstract
To determine whether or not the midbrain is involved in the control of ovulation, large mesencephalic lesions have been placed in 76 rats on the morning of proestrus, prior to the "critical period." When examined approximately 24 hours later, 52 of the lesioned rats had failed to ovulate as evidenced by the lack of tubal ova. Thirty-seven of these "blocked" animals were maintained until the morning of the 2d day after lesioning and 22 were still blocked; the remaining 15, however, had tubal ova, indicating that ovulation had''merely been delayed 24 hours. Fourteen rats which failed to ovulate by the 2d day following lesioning were examined at autopsy on the 3d day; 13 of these still had not ovulated. A comparison of the lesions responsible for the 3 types of results, i.e. no blockade, transient blockade or blockade for 2 or 3 days, revealed that the lesions associated with the failure to ovulate for 2 or 3 days involved an area of the brain stem that was not destroyed by the other lesions. The area that appears to be essential to ovulation is located ventro-medially in the mesodiencephalic junction. The portion of the mammillary peduncle located rostrally to the interpeduncular nucleus seems to fulfill most completely the anatomical criteria imposed by the lesion data. This and adjacent structures are discussed as to a possible role subserved in ovulatory mechanisms. No specific behavioral deficit was found to signal an "effective" lesion. The finding that massive destruction of the midbrain tegmentum and the resulting somnolence are compatible with ovulation seems to rule out the possibility that neural mechanisms underlying behavioral arousal are crucially involved in this neuroendocrine phenomenon. It may be that some other midbrain-diencephalic "activating system," unrelated to sleep-wakefulness, controls the cyclic release of pituitary ovulating hormone in this "spontaneously" ovulating form.