Adult male rats were maintained on 1 of 4 ad-lib diets: Group Control-Diet received a normal laboratory diet that contained no added chemicals; Group Lead-Diet received a diet containing 500 ppm (parts per million) lead; Group Cadmium-Diet received a diet containing 100 ppm cadmium; and Group Lead-Cadmium-Diet received a diet containing both 500 ppm lead and 100 ppm cadmium. After 60 days of exposure to their respective diets, animals were placed on restricted diets (15 g/day) of the identical food received during the exposure period. Each animal was trained to lever press on a fixed-interval 1-min schedule for 21 sessions (1 session/ day). The results of schedule training showed that lead alone or cadmium alone was associated with increased lever pressing relative to control diet. However, when lead and cadmium were exposed jointly, performance was not significantly different from control performance. Similar attenuation of effects were observed for central neurotransmitter functions. Specifically, disturbances in dopamine and serotonin turnover that were produced by lead alone were attenuated by the cotreatment of cadmium and lead. Possible accounts of the apparent antagonism between cadmium and lead are discussed.Because lead and cadmium are chemicals that continue to present health-related threats to humans and biota (Lansdown & Yule, 1986;Winter, 1982), the scientific community has focused attention on the toxicologic correlates of these trace metals. Regarding the neurotoxic effects associated with exposure to these contaminants, experimental inquiry has centered on toxicant-induced changes in neurotransmission. Inorganic lead, for example, is known to alter catecholaminergic function in the rat brain (see Winder & Kitchen, 1984, for a review). Although differential exposure routes and analytical techniques necessarily introduce some contradiction and ambiguity into this literature, the data are generally reliable in suggesting that low-level lead exposure enhances central catecholaminergic functions (Rossouw, Offermeir, & van Rooyen, 1987). By contrast, lead burdens are associated with deficits in central cholinergic functions (Shih & Hanin, 1978) and inhibited evoked release of peripheral acetylcholine (cf. Cooper & Manalis, 1983).With respect to cadmium contamination, low-level exposure consistently results in increased catecholamine neurotransmission