title: Neonatal lead exposure impairs development of rodent barrel field cortex.
abstract: Childhood exposure to low-level lead can permanently reduce intelligence, but the neurobiologic mechanism for this effect is unknown. We examined the impact of lead exposure on the development of cortical columns, using the rodent barrel field as a model. In all areas of mammalian neocortex, cortical columns constitute a fundamental structural unit subserving information processing. Barrel field cortex contains columnar processing units with distinct clusters of layer IV neurons that receive sensory input from individual whiskers. In this study, rat pups were exposed to 0, 0.2, 1, 1.5, or 2 g/liter lead acetate in their dam's drinking water from birth through postnatal day 10. This treatment, which coincides with the development of segregated columns in the barrel field, produced blood lead concentrations from 1 to 31 microg/dl. On postnatal day 10, the area of the barrel field and of individual barrels was measured. A dose-related reduction in barrel field area was observed (Pearson correlation = -0.740; P < 0.001); mean barrel field area in the highest exposure group was decreased 12% versus controls. Individual barrels in the physiologically more active caudoventral group were affected preferentially. Total cortical area measured in the same sections was not altered significantly by lead exposure. These data support the hypothesis that lead exposure may impair the development of columnar processing units in immature neocortex. We demonstrate that low levels of blood lead, in the range seen in many impoverished inner-city children, cause structural alterations in a neocortical somatosensory map.
authors.affiliation: Kennedy Krieger Institute and Department of Neurology, Johns Hopkins University, 707 North Broadway, Baltimore, MD 21205, USA. wilsonm@kennedykrieger.org
authors.forename: M A
authors.initials: MA
authors.lastname: Wilson
authors.forename: M V
authors.initials: MV
authors.lastname: Johnston
authors.forename: G W
authors.initials: GW
authors.lastname: Goldstein
authors.forename: M E
authors.initials: ME
authors.lastname: Blue
mesh_terms: D000284:Administration, Oral; D000818:Animals; D000831:Animals, Newborn; D004305:Dose-Response Relationship, Drug; D003576:Electron Transport Complex IV / Q000032:analysis; D005260:Female; D007774:Lactation; D007854:Lead / Q000097:blood; D007855:Lead Poisoning / Q000503:physiopathology*; D009942:Organometallic Compounds / Q000008:administration & dosage / Q000633:toxicity*; D051381:Rats; D020318:Rats, Long-Evans; D017207:Rats, Sprague-Dawley; D018091:Receptors, AMPA / Q000032:analysis; D017470:Receptors, Glutamate / Q000032:analysis*; D018094:Receptors, Metabotropic Glutamate / Q000032:analysis; D013003:Somatosensory Cortex / Q000187:drug effects / Q000254:growth & development* / Q000473:pathology; D014738:Vibrissae / Q000294:innervation*
chemical_list: D009942:Organometallic Compounds; D018091:Receptors, AMPA; D017470:Receptors, Glutamate; D018094:Receptors, Metabotropic Glutamate; C104723:glutamate receptor ionotropic, AMPA 3; C108822:metabotropic glutamate receptor 2; C102718:metabotropic glutamate receptor 3; D007854:Lead; D003576:Electron Transport Complex IV; C104722:glutamate receptor ionotropic, AMPA 2; C008261:lead acetate