An improved model of lead-induced brain dysfunction in the suckling rat

Experimental lead encephalopathy is produced in suckling rats when lead is added to the mother's diet. Lead passes into developing sucklings via maternal milk. Lead-poisoned newborns have been reported to exhibit pronounced retardation of growth and during week 4 of life develop paraplegia and extensive histologic lesions of the cerebellum. Under similar dietary conditions experimental lactating rats eat 30% less food than controls, resulting in: (a) sustained loss in body weight of nursing mothers and (b) offspring who develop paraplegia and cerebellar damage after gaining access to the maternal lead-containing diet.We have found that a lactating mother rat consuming 5% lead acetate (PbAc) in the diet (2.73% Pb) produced milk containing 25 ppm lead. When the diet of the mother is changed on day 16 from 5% PbAc to one containing 25 ppm Pb, and neonates are allowed free access to the same solid diet, the sucklings still have retarded body growth but do not develop paraplegia or grossly apparent vascular damage of the cerebellum. However, during week 4 these animals exhibit hyperactivity, tremors, and stereotype behavior. Pair-fed controls coetaneous to experimental groups do not display such activities. The severe paraplegia and histopathologic lesions reported by others in the older model obscures minimal brain dysfunction. We propose the present procedure as a model for studies of the subtle effects of lead on the central nervous system.