Effect of Postnatal Chronic Lead Exposure on Spatial Learning and Memory in Male Rat

Abstract

Background: Lead is a heavy metal with no apparent biological function. The widespread environmental contamination, the propensity to cause a wide spectrum of toxic effects and the number of individuals affected worldwide makes this ubiquitous neurotoxicant a public health problem of global magnitude. The nervous system is the primary target for the low levels of lead exposure and the developing brain appears to be especially vulnerable to lead neurotoxicity. Objectives: The aim of present study was to evaluate the effects of neonatal lead exposure on spatial learning and memory in Morris water maze. Materials and Methods: In this experimental study, 30 new born male rats were randomly divided into two groups: Control and lead exposure groups. Rat pups in lead exposure group received 8 mg/kg lead acetate intraperitoneally daily for 21 days. Then, rats trained with 6 trials per day for 6 consecutive days in the water maze at 36th postnatal day (PD). Twenty four hours after ending of training, a probe test was done to measure memory retention. Results: Results of this study demonstrated that exposure to lead could affect learning as indicating by significant differences in escape latency and traveled distance between 2 groups during 6 days of training. Lead exposure group exhibited significantly higher escape latency and distance traveled during training trials compared to control group. Also, lead exposure rats had higher platform location latency than control group during probe trial (P < 0.05). Conclusions: These data suggests that lead exposure during early postnatal period of brain development causes impairment in spatial learning and memory.

Prenatal and Postnatal Effect of Lead Acetate on the Histology of Frontal Cortex and Motor Activity in Wistar Rats

“…Pb is a highly neurotoxic agent affecting the developing central nervous system [6,7] through its interference of the cholinergic system and regulatory action of calcium on cell functions thereby disrupting many intracellular biological activities [8]. The alteration in this biochemical intercellular communication may precede neurobehavioral and neurological end points, usually observed in lead neurotoxicity [7].…”