Perinatal lead exposure alters postnatal cholinergic and aminergic system in rat brain: reversal effect of calcium co-administration

Our earlier studies indicated the role of neurotransmitter systems in lead (Pb) induced behavioral perturbations. In this study, we examined the alterations in synaptosomal acetylcholine (ACh), epinephrine, dopamine, acetylcholinesterase (AChE), and mitochondrial monoamine oxidase (MAO) in the cerebellum and hippocampus of perinatally Pb-exposed rats. Rats (Wistar) were exposed to 0.2% Pb (Pb acetate in drinking water of mother) from gestational day 6 and the pups were exposed lactationally (through mother's milk) to Pb till weaning (postnatal day 21). Studies conducted on different postnatal days (PND 21, 28, 35 and 60) showed significant decreases in synaptosomal AChE and mitochondrial MAO activities, and increases in the levels of ACh, dopamine and epinephrine in the cerebellum and hippocampus of Pb-exposed rats. These alterations were greater at PND 35 and more pronounced in the cholinergic system (ACh and AChE) of hippocampus and the aminergic system (epinephrine, dopamine and MAO) of cerebellum. The total locomotor activity and exploratory behavior were also decreased significantly in Pb-exposed animals corresponding to the alterations observed in cholinergic and aminergic systems. Calcium administration together with Pb, however significantly reversed the Pb-induced alterations in transmitters and enzymes, as well as exploratory and motor behavior suggesting protective effect of calcium in Pb-exposed animals.

► Pb-exposure altered AChE, MAO, ACh, dopamine and epinephrine levels.
► AChE and MAO decreased where as ACh, epinephrine and dopamine levels increased.
► Total locomotor activity and exploratory behavior decreased following Pb-exposure.
► Developing rats at PND 35 were found to be more vulnerable.
► Ca2+ supplement reversed significantly Pb-induced perturbations.