Abstract Previous studies from our laboratory indicate that somatosensory inputs to the snout and ventral trunk, but not visual or auditory stimuli, play critical roles in the elicitation and maintenance of maternal aggression by lactating Norway rats toward a strange male intruder. There are conflicting reports on the influence of olfaction on maternal aggression. We explored the possible roles of central or peripheral anosmia on maternal aggression in Long–Evans rats during early lactation. In Experiment 1, responsiveness to both volatile and non-volatile odors was eliminated by bilateral olfactory bulbectomy (BOB), carried out during mid-gestation. BOB resulted in a reduced likelihood and intensity of maternal aggression on days 1 and 5 of lactation (L1 and L5), but also severe deficiencies in maternal behavior and litter growth and survival. In Experiment 2, anosmia to volatile odors was induced by spraying zinc sulfate intranasally on gestation day 21 and L1. This treatment had little or no effect on maternal aggression on L1 or L2 or on maternal behavior, especially if there was a 1-day recovery between the second treatment and testing. In Experiment 3, responsiveness to non-volatile odors was eliminated by vomeronasal-organ removal (VNX) carried out prior to mating. VNX did not disturb maternal behavior on L2–L8 or maternal aggression on L1 or L5. These results and others suggest that the expression of maternal aggression is affected by volatile odors, mediated possibly by accessory chemosensory systems such as the septal organ, or by neural changes that follow olfactory deafferentation, or both.