title: Glial fibrillary acidic protein and RNA expression in adult rat hippocampus following low-level lead exposure during development.
abstract: The astroglial cytoskeletal element, glial fibrillary acidic protein (GFAP), is a generally accepted sensitive indicator for neurotoxic effects in the mature brain. We used GFAP as a marker for structural changes in rat hippocampus related to chronic low level lead exposure during different developmental periods. Four groups of rats were investigated: a control group, a perinatal group, which was exposed during brain development (E0-P16), a permanent group, exposed during and after brain development (E0-P100), and a postweaning group, exposed after brain development (P16-P100). Sections were processed for light microscopy (hematoxylin-eosin, Nissl, periodic acid Schiff (PAS) and GFAP-specific immunohistology), for electron microscopy, and for in-situ hybridization (GFAP). Sections were prepared from animals tested for active avoidance learning (AAL) and long-term potentiation (LTP). Chronic lead exposure did not affect glial and neuronal functions, as assessed by LTP and AAL, when lead exposure started after brain development (postweaning group). In this group, astrocytes displayed increased GFAP and GFAP gene transcript levels. However, lead exposure affected neuronal and glial function when the intoxication fell into the developmental period of the brain (perinatal and permanent groups). In these groups, LTP and AAL were impaired, and astrocytes failed to react to the toxic exposure with an adequate increase of GFAP and GFAP gene transcripts. Although GFAP is an accepted marker for neurotoxicity, our data suggest the marker function of GFAP to be restricted to postnatal toxic insult.
authors.affiliation: Institute of Neuropathology, Universitätsklinikum Benjamin Franklin, Berlin, Germany.
authors.forename: G
authors.initials: G
authors.lastname: Stoltenburg-Didinger
authors.forename: I
authors.initials: I
authors.lastname: Pünder
authors.forename: B
authors.initials: B
authors.lastname: Peters
authors.forename: M
authors.initials: M
authors.lastname: Marcinkowski
authors.forename: H
authors.initials: H
authors.lastname: Herbst
authors.forename: G
authors.initials: G
authors.lastname: Winneke
authors.forename: H
authors.initials: H
authors.lastname: Wiegand
mesh_terms: D000818:Animals; D005260:Female; D005904:Glial Fibrillary Acidic Protein / Q000096:biosynthesis*; D006624:Hippocampus / Q000187:drug effects / Q000196:embryology / Q000378:metabolism* / Q000648:ultrastructure; D007150:Immunohistochemistry; D007854:Lead / Q000633:toxicity*; D018811:Maternal Exposure; D008854:Microscopy, Electron; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D012333:RNA, Messenger / Q000096:biosynthesis*; D051381:Rats; D017208:Rats, Wistar
chemical_list: D005904:Glial Fibrillary Acidic Protein; D012333:RNA, Messenger; D007854:Lead