title: Histological study on hippocampus, amygdala and cerebellum following low lead exposure during prenatal and postnatal brain development in rats.
abstract: Neuropsychological studies in children who are exposed to lead during their early brain development have shown to develop behavioural and cognitive deficit. The aim of the present study was to assess the cellular damage in hippocampus, amygdala and cerebellum of rat pups exposed to lead during different periods of early brain development. Five groups of rat pups were investigated. (a) Control group (n = 8) (mothers of these rats were given normal drinking water throughout gestation and lactation), (b) pregestation lead-exposed group (n = 8) (mothers of these rats were exposed to 0.2% lead acetate in the drinking water for one month before conception), (c) gestation lead-exposed group (n = 8) (exposed to 0.2% lead acetate in the drinking water through the mother throughout gestation [gestation day 01 to day 21]), (d) lactation lead-exposed group (n = 8) (exposed to 0.2% lead acetate in the drinking water through the mother throughout lactation [postnatal day 01 to day 21]) and (e) gestation and lactation lead-exposed group (n = 8) (exposed to 0.2% lead acetate throughout gestation and lactation). On postnatal day 30, rat pups of all the groups were killed. Numbers of surviving neurons in the hippocampus, amygdala and cerebellum regions were counted using cresyl violet staining technique. Histological data indicate that lead exposure caused significant damage to neurons of hippocampus, amygdala and cerebellum regions in all lead-exposed groups except lactation lead-exposed group. The extent of damage to neurons of hippocampus, amygdala and cerebellum regions in lactation lead-exposed group was comparable to gestation and lactation groups even though the duration of lead exposure was much less in lactation lead-exposed group. To conclude, the postnatal period of brain development seems to be more vulnerable to lead neurotoxicity compared to prenatal period of brain development.
authors.affiliation: Department of Biochemistry, Melaka Manipal Medical College, Manipal University, Manipal, India.
authors.forename: Rajashekar Rao
authors.initials: RR
authors.lastname: Barkur
authors.affiliation: Department of Pharmacology, Kasturba Medical College, Manipal University, Manipal, India kl.bairy@manipal.edu.
authors.forename: Laxminarayana K
authors.initials: LK
authors.lastname: Bairy
mesh_terms: D000679:Amygdala / Q000187:drug effects* / Q000473:pathology; D000818:Animals; D002531:Cerebellum / Q000187:drug effects* / Q000473:pathology; D003072:Cognition Disorders / Q000139:chemically induced / Q000473:pathology; D005260:Female; D006624:Hippocampus / Q000187:drug effects* / Q000473:pathology; D007854:Lead / Q000633:toxicity*; D008297:Male; D018811:Maternal Exposure / Q000009:adverse effects; D009474:Neurons / Q000187:drug effects / Q000473:pathology; D020258:Neurotoxicity Syndromes / Q000209:etiology / Q000473:pathology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar
chemical_list: D007854:Lead
keywords: Developing brain; amygdala; blood lead; cerebellum; hippocampus; lead acetate