title: Developmental lead exposure disturbs expression of synaptic neural cell adhesion molecules in herring gull brains.
abstract: Neurobehavioral testing of herring gull chicks (Larus argentatus) in both laboratory and field studies indicates that lead exposure during critical periods of development causes neurological deficits that may compromise survival in the wild. Accumulating evidence suggests that lead impairs neurodevelopment, in part, by altering the expression of cell adhesion molecules (CAMs) responsible for the proper formation and maintenance of neural structure and synaptic function. We examined the adhesion molecules NCAM, L1, and N-cadherin in gull brains to determine whether these CAMs are altered by lead exposure and might serve as markers of developmental neurotoxicity. One-day-old chicks were collected from nesting colonies and were laboratory housed. On post-hatching day (PHD) 2, chicks were given 100 mg/kg lead acetate or saline (intraperitoneally). Birds were killed on PHD 34, 44, or 55 (blood-lead levels averaged 27.4, 20.8, and 19.5 microg/dl, respectively). Brains were removed and stored at -70 degrees C until analysis. Expression of CAMs was determined in synaptosomal preparations by Western blotting and the activity of NCAM-associated sialyltransferase (ST) was determined in purified whole brain golgi apparatus. Elevation in synaptosomal polysialylated NCAM expression and a significant increase in golgi ST activity was observed in lead-treated animals at PHD 34. Reductions in synaptosomal N-cadherin were observed at PHD 34 and 44, while L1 expression appeared unaffected by lead at any time-point. By 55 days post-hatching, no differences in N-cadherin expression, polysialylated NCAM expression or NCAM-associated ST activity were seen in lead-treated animals as compared with age-matched control animals. Lead-induced disruption of CAM expression during early neurodevelopment may contribute to behavioral deficits observed in herring gulls in both the laboratory and the field, and may serve as a marker for heavy metal exposure during postnatal development.
authors.affiliation: Neurotoxicology Laboratories, Rutgers University, 41B Gordon Road, Piscataway, NJ 08854-0789, USA.
authors.forename: P M
authors.initials: PM
authors.lastname: Dey
authors.forename: J
authors.initials: J
authors.lastname: Burger
authors.forename: M
authors.initials: M
authors.lastname: Gochfeld
authors.forename: K R
authors.initials: KR
authors.lastname: Reuhl
mesh_terms: D000818:Animals; D015415:Biomarkers; D001717:Birds / Q000378:metabolism*; D015153:Blotting, Western; D001923:Brain Chemistry / Q000187:drug effects*; D015820:Cadherins / Q000378:metabolism; D003720:Densitometry; D007854:Lead / Q000097:blood; D020263:Lead Poisoning, Nervous System / Q000378:metabolism*; D019006:Neural Cell Adhesion Molecules / Q000096:biosynthesis*; D012799:Sialyltransferases / Q000378:metabolism; D013347:Subcellular Fractions / Q000737:chemistry / Q000378:metabolism; D013569:Synapses / Q000187:drug effects / Q000378:metabolism*; D013574:Synaptosomes / Q000187:drug effects / Q000378:metabolism
chemical_list: D015415:Biomarkers; D015820:Cadherins; D019006:Neural Cell Adhesion Molecules; D007854:Lead; D012799:Sialyltransferases