1. Polychlorinated biphenyls (PCB) were released into the environment through improper disposal for decades, causing widespread contamination. Slow biodegradation and lipophilic properties of PCB caused its persistence and concentration through food webs. Exposure to these environmental contaminants through maternal transfer during early development has been associated with neurological and endocrinological alterations in several different organisms. 2. The present study extended a preliminary investigation which suggested low level exposure to PCB altered acetylcholine biosynthesis enzyme, choline acetyltransferase (ChAT), activity in the hippocampus and basal forebrain and caused aberrations in thyroid hormone and behavior. 3. Dietary exposure of 15-day-old animals to 1.25 ppm of Aroclor 1254 (LPCB) during gestation and lactation significantly elevated ChAT activity in both areas of the brain. Animals exposed to 12.5 ppm of Aroclor 1254 (HPCB) until 15 days of age demonstrated significant elevations of ChAT activity in the basal forebrain. Thyroxine (T4) concentrations were slightly elevated in 15-day-old LPCB animals and significantly depressed in HPCB exposed pups; triiodothyronine (T3) concentrations were not altered. 4. At 30 days both LPCB and HPCB treatment groups displayed significantly depressed ChAT activity in both areas of the brain. T3 and T4 concentrations were subnormal, although T4 was not significantly depressed in LPCB animals. 5. In the Morris water maze all animals, when tested between 25 and 29 days of age, improved their latency time to the platform over 10 spatial learning trials. However, when combined means of trials 8-10 were compared, HPCB exposed animals had significantly increased latency time to the podium compared to control and LPCB animals.