Lordosis responses in naturally-estrous hamsters were elicited by unilateral manual stimulation. Response latencies were compared before and after unilateral lesions of medial and lateral tegmental areas located ventral and ventrolateral, respectively, to the midbrain central gray. The only significant effects were produced by the more lateral lesions. These caused slightly delayed lordosis responses to stimulation of the ipsilateral flank, but had much more pronounced effects on responsiveness to contralateral stimuli, which often entirely failed to elicit lordosis postlesion. This difference in the effectiveness of ipsi- and contralateral stimuli suggests a selective disruption of neural mechanisms involved in the somatosensory control of lordosis initiation. Its locus suggests that a similar mechanism previously identified in the hamster tectum extends ventrally into the dorsal tegmentum, where it overlaps areas implicated in the sensory control of lordosis in other rodents. Since unilateral lesions of the dorsomedial tegmentum failed to affect behavior, a second experiment tested the effects of bilateral medial lesions on male-stimulated lordosis responses in ovariectomized, hormone-primed hamsters. These lesions caused significant increases in body weight, but again failed to show direct effects on lordosis. This result helps to delimit a ventral tegmental system previously implicated in the control of lordosis maintenance in hamsters. In addition, it suggests species differences in the brain circuits involved in the motor control of lordosis.