Effect of Pb‐acetate on neurobehavior and learning in the kitten

Abstract

Pb‐induced learning and behavioral deficits, and hypo‐spiny neurons of the motor cortex, cerebellum, and hippocampus, do not occur in rats until blood‐lead levels (BLLs) reach at least 21 μg/dL. In contrast, elevated aggression and poor intelligence scores occur in children with BLLs lower than 10 μg/dL. Similarly, Pb‐exposed kittens show increased aggression with BLLs less than 10 μg/dL, which may be associated with Pb‐induced hyper‐spiny neurons of the motor cortex, hippocampus and cerebellum. These results suggest that Pb ingestion by kittens will result in learning and behavioral deficits similar to those observed in lead‐burdened children. To test this, kittens were treated (20 mg/kg/day, lead acetate or equal volume distilled water via esophageal intubation) from post natal day 1 to 7. At 8‐ and 10‐weeks of age, the kittens were tested in a reversal t‐maze, an open field, and a free fall test. Eight‐week‐old Pb‐treated kittens showed a delay in learning as demonstrated by a significant higher number of incorrect arm choices in the t‐maze that returned to control levels when the kittens reached 10‐weeks of age. No differences occurred between treatment groups at 8‐ and 10‐weeks of age in the open field or free fall tests. These results show the kitten to be a viable model for Pb toxicity studies in that it better simulates the effects of Pb toxicity found in children. Supported by an Institutional Graduate Program Grant.